Cardiology

101. Which one of the following is characteristic of atrial myxoma? Usually originates in the right atrium Fragments of tumour easily break off and grow in its peripheral sites Echocardiogram is diagnostic in most cases !he clinical signs can mimic se"ere mitral regurgitation #ecurrence is fre$uent e"en after successful surgical remo"al of the tumour

our answer

%trial myxoma is a benign tumour of the heart. %pproximately &'( originate in the left atrium. !he clinical features are characterised by a triad of embolism) intracardiac obstruction and constitutional symptoms. !he clinical signs can mimic mitral stenosis and the murmur may "ary with body position. Fragments of tumour easily break off but do not grow in its peripheral sites. %fter complete and careful remo"al of the tumour recurrence is "ery rare.

10*. % *+,year,old man presents with a *,year history of increasing dyspnoea with strenuous exertion. -ypertrophic cardiomyopathy is diagnosed. Which is the most appropriate screening method for his brother? .omputed tomography /.!0 scan Exercise tolerance test 1entilation2perfusion scan Echocardiography 3enetic screening

our answer

-ypertrophic cardiomyopathy is usually familial with autosomal dominant transmission. !he diagnosis of hypertrophic cardiomyopathy is based upon the demonstration of unexplained myocardial hypertrophy) which is best done using two,dimensional echocardiography. !he diagnosis re$uires that measurements of wall thickness exceed two standard de"iations for sex,) age,) and si4e,matched populations. 5n practice) in an adult of normal si4e) the presence of a left "entricular myocardial segment of 1.' cm or greater in thickness) in the absence of a recognised cause) is usually considered to be diagnostic. 6ess stringent criteria should be applied to first,degree relati"es of an affected indi"idual) where the probability of carrying the disease gene increases from 17'00 to 17*.

108. % *',year,old woman is seen in outpatients and is found to ha"e loud first heart sound) an early diastole sound followed by a mid,diastolic murmur. What is the likely diagnosis? 9itral stenosis with a fourth heart sound 9itral stenosis with atrial fibrillation 9itral stenosis with mobile leaflets 9itral stenosis with pulmonary hypertension 9itral "al"e prolapse

our answer

From the information gi"en) the diagnosis is mitral stenosis with mobile leaflets. !here is no information regarding atrial fibrillation or pulmonary hypertension. :pening snap indicates that the mitral "al"e is mobile. !he snap occurs when the superior systolic bowing of the anterior mitral "al"e leaflet is rapidly re"ersed towards the left "entricle in early diastole) due to the high left atrial pressure. ;< is classically late diastolic or presystolic. 5t occurs when augmented atrial contraction causes presystolic "entricular distension so that the "entricle then contracts with greater force. %trial myxoma can produce an early diastolic sound /tumour plop0) which is due to the abrupt diastolic seating of the tumour within the right or left atrio"entricular orifice.

10<. A 50-year-old woman is referred to out-patients for a previously asymptomatic atrial septal defect (ASD). She is new to the area and was last seen around 6 years ago in her previous local hospital. She is a smo er !ut without other significant medical history. She now complains of shortness of !reath on e"ertion# together with peripheral oedema. $linical e"amination reveals her to !e clu!!ed and cyanosed. %er pulse rate is &0 !pm and !lood pressure &'(60 mm%g. )cho demonstrates a dilated right heart with an estimated right ventricular pressure of &0 mm%g and significant tricuspid and pulmonary regurgitation. *hat is the li ely diagnosis+ $or pulmonale )isenmenger,s syndrome our answer -nfective endocarditis

.rimary pulmonary hypertension .ulmonary em!oli disease

/his woman has developed massive irreversi!le pulmonary hypertension as a conse0uence of a previous left to right shunt. .ulmonary pressures have now reached systemic level. /he reversal of a left to right shunt as a conse0uence of pulmonary hypertension is nown as )isenmenger,s syndrome# and is generally the result of a previously undiagnosed ASD# ventricular septal defect (1SD) or patent ductus arteriosus. -t may also result from an incompletely corrected 2allot,s tetralogy or )!stein,s anomaly. .rognosis is poor# although a few patients may !e candidates for heart3lung transplantation. Symptomatic treatment is directed towards right heart failure. $omplications include polycythaemia# !leeding disorders and cere!ral em!olism or a!scess. Since there is a particularly high ris in those of child!earing age# patients should !e given appropriate advice and information to avoid pregnancy.

10'. A 40-year-old woman is admitted with chest pain and !reathlessness. 5n e"amination# her heart rate is 640 !eats(min. )$7 shows atrial fi!rillation. *hat is the ne"t step in her management+ Administration of propranolol Administration of verapamil Asynchronous cardioversion Administration of warfarin -mmediate heparinisation our answer /he appropriate treatment for atrial fi!rillation (A2) is determined !y the patient,s relative ris from the arrhythmia. %igh-ris patients include those with

a heart rate greater than 650 !eats(min# chest pain# an unsta!le condition or shoc . /hese patients re0uire urgent treatment. -mmediate heparinisation# to reduce the ris of systemic em!olisation# and attempted cardioversion with synchronised D$ shoc should !e carried out first. *arfarin treatment is indicated in the elderly and those with heart disease. 8oung patients with lone atrial fi!rillation in the a!sence of heart disease may not need anticoagulation.

10=. Which of the following conditions is most likely to produce a wide) relati"ely fixed split of ;*? .ongesti"e cardiac failure 6eft bundle,branch block 9oderate "entricular septal defect #ight bundle,branch block and heart failure Wolff2>arkinson2White syndrome

our answer

#??? makes the split wide and the heart failure fixes the split. /-eart failure does not permit much of a change in "entricular "olume with respiration) because breathing with congested lungs is shallow.0 #ight "entricular failure /#1F0 secondary to pulmonary hypertension />-!0 is another condition where you can get a wide fixed split) the wideness of the split being due to a prolonged iso"olumetric contraction time in the failing right "entricle. 5n cases of moderate "entral septal defects) the widening is due to delayed >*) but it is not fixed. 5n W>W and other causes of electrical delay of 61 conduction) including 6???) there is a narrowly split ;*.

10&. % young man comes to the % @ E Aepartment complaining of feeling unwell and palpitations. ;upra"entricular tachycardia is confirmed on E.3 and he responds to carotid sinus massage. ;ubse$uently) the E.3 shows a ># inter"al of 0.0B sec) widened C#; complex in all leads with a slurred upstroke) dominant # wa"e in 11 and left axis de"iation. What is the most likely diagnosis? #heumatic fe"er Wolff2>arkinson2White syndrome %trial fibrillation %;A #ight bundle,branch block

our answer

!he E.3 features are typical of Wolff,>arkinson,White /W>W0 syndrome. !his condition is classically associated with a short ># inter"al /D 0.1* s0. ;lurring of the C#; complex is due to an extra wa"e called a delta wa"e. %s the %1 node and bypass tract ha"e different conduction speeds and refractory periods) a re,entry circuit can de"elop) causing paroxysms of tachycardia. .arotid sinus massage or intra"enous adenosine will often terminate an episode of this form of tachycardia. :ne of the features of myocarditis due to rheumatic fe"er is a prolonged ># inter"al. !his occurs due to a first, or second,degree block. 5n atrial fibrillation) the E.3 shows normal but irregular C#; complexesE there are no > wa"es but the baseline may show irregular fibrillation wa"es. % right bundle,branch block presents with wide C#; complexes) dominant # in lead 11) in"erted ! wa"es in 11 2 1< and a deep wide ; wa"e in lead 1=. %trial septal defects are usually associated with a right bundle,branch block. !his leads to an r;# pattern

10+. % '0,year,old woman who is already on ramipril) frusemide and atenolol for heart failure) decompensates and presents to %@E with pulmonary oedema. -er heart rate is 1*0 bpm and her blood pressure is 100F=' mm-g. ;he is gi"en oxygen and diamorphine. Which of the following actions is indicated in her further management? 5ncrease diuretics and maintain the current dose of G,blocker 5ncrease diuretics) reduce the G,blocker dose 5ncrease diuretics) increase the G,blocker dose 5ncrease diuretics) stop G,blockers and later increase the G,blocker dose when her lungs are dry 5ncrease diuretics) stop G,blockers and restart G,blockers when her lungs are dry %lthough G,blockers are not started for the first time in a patient with pulmonary oedema) in a case like this) when the patient is already on G,blockers) it is wise to carry on with the same dose. our answer

10B. % &*,year,old man was discharged following successful prosthetic aortic "al"e replacement. %part from a small 1enflon abscess) which healed with appropriate dressings and cannula remo"al) his progress had been unremarkable. How) some = weeks later) he is brought to %@E by his wife) suffering from malaise) fe"er and night sweats. :n examination you can hear the murmur of his prosthetic heart "al"e. ?lood testing re"eals mild anaemia and raised E;#. !ransoesophageal echocardiography suggests the possibility of "egetations. Which of the following regimens is the most appropriate initial choice of antibiotic therapy?

5ntra"enous penicillin therapy 5ntra"enous gentamicin therapy 5ntra"enous penicillin and gentamicin 5ntra"enous "ancomycin) rifampicin and gentamicin our answer 5ntra"enous gentamicin and "ancomycin !he choice of antibiotics to treat endocarditis should be guided by local policy) but in the case of possible prosthetic "al"e endocarditis) regime A is the most appropriate. #egime . is the most appropriate initial therapy for non,prosthetic "al"e endocarditis. Early prosthetic "al"e endocarditis is usually caused by Staphylococcus epidermidis, occurring during the first * months post"al"e replacement) other causati"e organisms include Staphylococcus aureus) 3ram,negati"e bacilli) diphtheroids and Candida species. 5n patients with prosthetic "al"es) transthoracic echocardiography is less sensiti"e than transoesophageal echo for detecting "al"e abnormalities. Unfortunately medical therapy is rarely successful in prosthetic "al"e endocarditis) and surgical "al"e replacement under antibiotic co"er is usually re$uired.

110. % &*,year,old woman presents with two syncopal episodes) and is brought to the Emergency department by her daughter. !he second episode has occurred on a particularly hot day after a family walk. ;he has a past history of hypertension and takes bendroflua4ide. :n admission to Emergency her blood pressure is 1=0F1*' mm-g and there is an eIection systolic murmur on auscultation of her chest that radiates to the carotids. What diagnosis best fits with this clinical picture? 9itral regurgitation -ypertrophic cardiomyopathy %ortic stenosis our answer %cute arrhythmia Aehydration due to diuretic use %ortic stenosis causes left "entricular outflow obstruction) which is manifest by a rough eIection systolic murmur) best heard at the base of the heart) and transmitted to the carotids. %s aortic stenosis becomes more se"ere) the sound of aortic "al"e closure begins to diminish in intensity. !here is associated left "entricular hypertrophy) with narrowing of the pulse pressure in the later stages of aortic stenosis. ;ymptoms commonly appear when the "al"e orifice decreases to less than 1 cm s$uared /normal orifice is 8 cm s$uared0. ;tenosis is considered se"ere when the orifice is less than 0.' cm s$uared or the pressure gradient across the "al"e is '0 mm-g or greater. ;ymptoms of aortic stenosis include angina) syncope /particularly exertional0 and congesti"e heart failure. 35 bleeding may occur) as there is an association between aortic stenosis and haemorrhagic telangiectasia.

5n"estigations of choice are chest x,ray and Echocardiography) with cardiac catheterisation in symptomatic patients to assess the gradient across the "al"e. ;urgical "al"e replacement is the treatment of choice in appropriate patients.

111. %n %sian boy with a known history of rheumatic heart disease presents with low, grade fe"er for the past month. -e recei"ed a course of antibiotics from his 3> a week ago. Which of the following in"estigations would be most useful in the diagnosis? ?lood culture ;erological testing Echocardiogram .,reacti"e protein Full blood count

our answer

Echocardiography is extremely useful in allowing "egetations in infecti"e endocarditis to be seen. %lthough blood cultures are a key diagnostic test in this condition) they may be negati"e if patients ha"e recently recei"ed antibiotic therapy. !he same reasoning applies to serological tests for Coxiella, Bartonella, Legionella, Chlamydia and Brucella spp that may also cause infecti"e endocarditis. ?oth .#> and polymorphonuclear leucocytosis are non, specific tests.

11*. % 8+,year,old woman is seen in %@E with a history of collapse. ;he recalls rushing for the bus before feeling faint. -er brother recently died suddenly due to a heart problem. :n examination she has a JIerkyK pulse) a thrusting cardiac impulse and a mid,systolic murmur. What is the likely diagnosis? Ailated cardiomyopathy -ypertrophic cardiomyopathy 9itral "al"e prolapse %ortic stenosis >ericarditis

our answer

-ypertrophic cardiomyopathy /-.90 is the commonest form of cardiomyopathy) with a pre"alence of about 100 per 100)000. 5t is a genetic disorder with autosomal,dominant transmission) a high degree of penetrance and "ariable expression. ;ymptoms and signs are similar to those of aortic stenosis) except that the character of the pulse in -.9 is Ierky. !he age of the patient and her family history make -.9 the likely diagnosis.

;udden death can be a presenting symptom. 5t typically occurs during or Iust after "igorous physical acti"ity. #isk factors for sudden death in -.9 are7 L a history of pre"ious cardiac arrest or sustained "entricular tachycardia L recurrent syncope L an ad"erse genotype andFor family history L exercise,induced hypotension L multiple episodes of non,sustained "entricular tachycardia on ambulatory E.3 L a marked increase in the thickness of the left "entricular wall

118. %n 1+,year,old man with 9arfanKs syndrome is re"iewed in the cardiology clinic. Which cardiac abnormality is most likely to be found? %ortic regurgitation %trial septal defect Ailated cardiomyopathy 9itral "al"e prolapse >ersistent ductus arteriosus our answer

9arfanKs syndrome is characteristically associated with progressi"e aortic root dilatation leading to aortic regurgitation and an increased risk of dissection. :ther skeletal manifestations include tall stature) scoliosis) chest wall malformations) high arched palate and lens dislocation. 9itral "al"e prolapse is also common but there is no association with other congenital malformations or cardiomyopathy.

11<. % 1=,year,old young man had a cardiac arrest while playing football and was resuscitated. -e reco"ered fully and was later found to ha"e -:.9 /hypertrophic obstructi"e cardiomyopathy0. Which is the best treatment option? 5mplantable cardio"erter defibrillator %miodarone G,?lockers 1erapamil #ate,responsi"e) dual,chamber pacemaker our answer

For the secondary pre"ention of sudden cardiac death /;.A0 in patients with -:.9) there is e"idence and general agreement that 5.A is the most useful option. E"en for the primary pre"ention of ;.A in -:.9) the weight of e"idence is currently in fa"our of its efficacy) although in selected patients amiodarone has a role. :ptions .) A and E are not considered effecti"e in pre"enting ;.A in -:.9.

11'. Which of the following pharmacological agents is most likely to benefit a patient with angina due to syndrome M? %spirin ?isoprolol Aia4epam Ailtia4em 5sosorbide mononitrate

our answer

Hitrates are often effecti"e in patients with syndrome M. .ardiac syndrome M consists of angina,like chest pain during exertion) characteristic E.3 changes during exercise testing) normal coronary arteries on cardiac catheterisation and no inducible coronary artery spasm during catheterisation. 5t should not be confused with the metabolic syndrome M) which comprises central obesity) glucose intolerance) dyslipidaemia) and high blood pressure. !he dyslipidaemia in this case is primarily high triglycerides and low -A6 cholesterol. >eople with metabolic syndrome are at increased risk of coronary artery disease.

11=. % &',year,old male patient with type,* diabetes mellitus is brought to %@E complaining of chest pain. -e was discharged * days ago after an une"entful hospital course following an acute 95 1 N weeks pre"iously) ha"ing been successfully thrombolysed with streptokinase. %n E.3 in %@E shows ;! ele"ations in leads 11218. !he patient has been gi"en 10 U reteplase i". Which of the following statements is correct regarding the further management of this patient? !he dose of reteplase should not be repeated ;treptokinase would ha"e been a better choice in this situation %ntithrombins like heparin should not be administered with reteplase .linical trials show that streptokinase gi"es the maximum thrombolytic patency rates !he thrombolytic agent associated with the minimum risk of haemorrhagic stroke is streptokinase

our answer

!he thrombolytic agents appro"ed for use in the UO by the Hational 5nstitute of .linical Excellence /H5.E0 are streptokinase) reteplase) tenecteplase and alteplase. ;treptokinase is gi"en as an i" infusion o"er 1 hour. !enecteplase is gi"en as a single bolus inIection. #eteplase is gi"en as two i" boluses 80 minutes apart. %lteplase is gi"en either as an accelerated regimen /one bolus followed by two i" infusions0 or as a standard regimen /one bolus and fi"e infusions0. 5f streptokinase had been gi"en more than ' days ago) neutralising antibodies may pre"ent the efficacy of a second dose and another agent should be used. .linical trials ha"e shown that the maximum B0,minute patency rate is obtained with reteplase. 9ost trials ha"e shown no significant difference in mortality rates between the "arious thrombolytic agents. -owe"er) 3U;!: 1 showed that the accelerated alteplase regimen was superior to streptokinase. %;;EH! * found almost e$ual 80,day mortality rates associated with the tenecteplase and accelerated alteplase regimens. !hus accelerated alteplase and tenecteplase are belie"ed to be superior to streptokinase. !he thrombolytic agent with the minimum risk of causing haemorrhagic stroke is streptokinase. -eparin is co,administered with reteplase and alteplase) but not with streptokinase.

11&. ou re"iew a =+,year,old woman who presents with a sudden episode of collapse while taking communion in church. !his has been her third syncopal episode. >ast medical history of note includes recently diagnosed se"ere hypertension) for which her 3> has commenced enalapril therapy. :n examination her blood pressure is 1=0F180 mm-g) she has left "entricular hypertrophy on clinical examination and a loud eIection systolic murmur. %uscultation of the chest re"eals bibasilar crackles consistent with mild heart failure. Which of the following is the definiti"e in"estigation of choice for this patient? .hest M,ray Electrocardiogram /E.30 Echocardiogram .ardiac catheterisation *< h holter monitor

our answer

!his patient is suffering from symptomatic aortic stenosis as e"idenced by the history of syncope) hypertension) left "entricular hypertrophy and harsh eIection systolic murmur. While echocardiography will aid in diagnosis) gradient across the aortic "al"e may be underestimated because of the possibility of multiple echo signals and co,existent left "entricular dysfunction. %s such cardiac catheterisation is the definiti"e in"estigation as it allows for more accurate estimation of "al"e gradient and characterisation of co,existent coronary artery disease) which may re$uire inter"ention at the same time.

11+. Which en4yme synthesises phosphodiester bonds as part of AH% replication) repair and recombination processes? AH% gyrase AH% ligase our answer AH% polymerase AH% photolyase AH% glycolyase AH% ligase synthesises phosphodiester bonds. AH% gyrase is a type,* topoisomerase of Escherichia coli. AH% polymerase synthesises AH% on a AH%F#H% template. AH% photolyase is a bacterial en4yme in"ol"ed in photoreacti"ation repair. AH% glycolyase takes part in base excision and mismatch repair processes.

11B. % &*,year,old man presents with 1' min of central crushing chest pain. E.3 shows 0.' mm ;! ele"ation in leads 11 and 1*. ou are in a peripheral hospital with no acute cardiac catheterisation lab. What is the most appropriate treatment? %ccelerated tissue plasminogen acti"ator /t>%0 P aspirin %spirin P heparin and repeat electrocardiogram /E.30 in 1' min -eparin only Ho treatment and repeat E.3 in 1' min ;treptokinase P aspirin

our answer

!he criteria for thrombolysis are 1 mm ;! ele"ation in two or more limb leads or * mm ;! ele"ation in adIacent chest leads) so thrombolysis is not indicated here. -owe"er) in the context of a good history of cardiac pain and borderline E.3) an acute coronary e"ent should be strongly suspected and aspirin and heparin gi"en prophylactically) with a repeat E.3 in 1' min.

1*0. % **,year,old student is admitted by ambulance from a local night club. -e has no pre"ious medical history of note and is adopted so is unaware of his family history. ?ystanders who ha"e accompanied him say that he suffered sudden collapse while dancing. ?ouncers at the club claim that they couldnKt feel a strong pulse during his period of unconsciousness. :n admission his blood pressure is 1*0F=0 mm-g) and pulse is +0 bpm and regular. E.3 looks normal) corrected C! inter"al is 0.= s. What diagnosis fits best with his clinical picture?

;imple syncope 6ong C! syndrome 2 mutation uncharacterised our answer Ecstasy o"erdose .arotid sinus syndrome Qer"ell26ange,Hielsen /Q6H0 syndrome !his manKs C! inter"al is prolonged. Q6H syndrome is also associated with long C!) but patients ha"e deafness in addition to the cardiac rhythm abnormality. Episodes of se"ere C! prolongation and torsades de pointes "entricular tachycardia in congenital long C! syndrome may be precipitated by increased adrenergic dri"e /such as that from dancing in a night club0. !his patient is adopted) so that it may be possible that there is an unknown family history of sudden death. !he molecular biology of long C! syndromes is heterogeneous) and a number of different mutations coding for potassium or sodium channels may be responsible. Where specific mutations are identified) antiarrhythmic therapy may be specifically targeted to pro"ide optimum therapy. 5n patients who respond poorly to medical treatment) implantable defibrillator may be considered.

1*1. A 60-year-old man suffered an anterior myocardial infarction. %e had all the ris factors for coronary artery disease. *hich of the following nonpharmacological interventions will !e most helpful in reducing his ris of a future ischaemic event+ A2 duration less than 6 months prior to cardioversion Diet control 9egular e"ercise Stopping smo ing our answer *eight reduction All these interventions are effective !ut stopping smo ing is the single most effective# non-pharmacological intervention that will help to reduce the ris of a future event. /here are trials showing that smo ing cessation is as effective as having a coronary artery !ypass graft.

1**. An 6'-year-old young man presents to A:) having developed palpitations while playing foot!all. )$7 shows rapid atrial fi!rillation with a ventricular rate of around ;50 !pm. <9S duration is prolonged at around 6=0 ms. D$ cardioversion is performed. Su!se0uent )$7 in sinus rhythm demonstrates a .9 interval of 600 ms# positive 9 wave in 16 and the presence of a delta wave. *hat further treatment would you recommend+ Atrial defi!rillator implantation -ntravenous and then oral loading with amiodarone 9adiofre0uency a!lation of the accessory pathway our answer 9adiofre0uency a!lation of the A1 node Surgical a!lation of the accessory pathway /his young man has *olff3.ar inson3*hite (*.*) syndrome. /he most common arrhythmia is an atrioventricular re-entry tachycardia (A19/). /his is a narrow comple" with anterograde conduction through the A1 node and retrograde conduction via the accessory pathway. .atients who develop A2 are at ris of rapid anterograde conduction to the ventricles via the accessory pathway# and this may su!se0uently degenerate to 12. /he e"tremely rapid conduction with !road <9S duration is typical of this complication. 9adiofre0uency a!lation of the accessory pathway is recommended in this setting and is potentially curative.

1*8. % '+,year,old man is ha"ing his drug therapy re"iewed following a myocardial infarction. Which of the following has no pro"en benefit on mortality following myocardial infarction /950?

%tor"astatin 5sosorbide mononitrate #amipril !imolol !irofiban

our answer

!he glycoprotein 55bF555a antagonist tirofiban />#5;9,>6U;0) timolol /!595 trials0 and ramipril /%5#E0 ha"e all been shown to reduce mortality following myocardial infarction. !he recent 95#%.6 study showed that ator"astatin reduced cardio"ascular e"ents by 1&( when gi"en for three months post,95. 5sosorbide mononitrate showed no benefit in the 5;5; < study.

1*<. 9ight ventricular myocardial infarction is characterised !y which of the following+ S/-segment elevation in leads --# --- and a12 with < waves and /wave inversion in these leads 5cclusion of the left coronary artery >ar ed pulmonary vascular congestion A rise in systolic !lood pressure A!sent ?ussmaul,s sign 9ight ventricular myocardial infarction usually occurs in association with an inferior-wall left ventricular infarction# as revealed !y the )$7. /here is usually a right coronary occlusion. $haracteristic clinical features include a low cardiac output syndrome with @ugular venous distension !ut no pulmonary vascular congestion. ?ussmaul,s sign (increased @ugular venous distension with inspiration) may !e evident. our answer

1*'. % '<,year,old man is <+,h postmyocardial infarction. ou are asked to re"iew him as he is suffering worsening cardiac failure. :n examination he has a pansystolic murmur)

loudest at the apex. What complication of his myocardial infarction is most likely to ha"e occurred? 1entricular septal defect %trial septal defect %cute mitral regurgitation our answer %cute pulmonary regurgitation 1entricular rupture %cute mitral regurgitation associated with myocardial infarction may occur due to ruptured chordae tendineae. :ther causes of mitral regurgitation include papillary muscle dysfunction) infecti"e endocarditis) rheumatic heart disease) idiopathic myxomatous "al"e degeneration) left atrial myxoma) systemic lupus erythematosus /;6E0 and drugs /fenfluramine and dexfenfluramine0. !he in"estigation of choice is echocardiography) which may identify left atrial and left "entricular dilatation and confirm the diagnosis of chordae tendineae rupture. 9itral regurgitation associated with chordal rupture in 95 may be catastrophic and re$uire emergency surgery for "al"e replacement. %cute medical management in"ol"es treatment with angiotensin,con"erting en4yme /%.E0 inhibition) diuretic therapy and possible anticoagulation. !he prognosis for patients with mitral regurgitation is generally good) except in the post,95 situation.

1*=. A =0-year-old woman presents with a three month history of chest pain. 5n auscultation# there is a midsystolic clic and a late systolic murmur. %er electrocardiogram shows /-wave inversions in leads --# ---# and a12. *hich of the following statements concerning her condition is true+ /he woman,s chest pain could !e due to associated coronary artery disease /he clic and murmur is li ely to occur earlier in systole when the patient stands An e"ercise stress test would most li ely !e positive Asymmetrical hypertrophy of the interventricular septum is revealed on echocardiography .rophylactic measures to prevent su!acute !acterial endocarditis are not warranted

our answer

/he systolic clic -murmur syndrome is associated with mitral valve prolapse. -t occurs in appro"imately AB of the normal asymptomatic population. -t can place e"cessive stress on the papillary muscles and lead to ischaemia and chest pain. Although often associated with inferior /wave changes# the systolic clic -murmur syndrome only occasionally results in an ischaemic response to e"ercise. 5n standing or during the 1alsalva manoeuvre# as ventricular volume gets smaller# the clic and murmur move earlier in systole. )chocardiography reveals midsystolic prolapse of the posterior mitral leaflet or# on occasion# !oth mitral leaflets into the left atrium. Asymmetrical hypertrophy of the interventricular septum is a feature of hypertrophic o!structive cardiomyopathy (%5$>). -nfective endocarditis prophyla"is is necessary for those patients with a murmurC an isolated mid-systolic clic does not merit them.

1*&. A AA-year-old man presents with a ;-hour history of severe central chest pain. )$7 shows S/ elevation in the anterior leads. %e was recently discharged following a laparotomy for intestinal o!struction. *hat would !e the !est line of treatment for him+ Aspirin and clopidogrel Strepto inase $oronary angioplasty our answer -ntravenous heparin Alteplase /he symptoms and investigations suggest an acute anterior myocardial infarction. Although throm!olysis would !e the normal course of treatment# it would have to !e deferred in this case !ecause of his recent ma@or surgery. Aspirin and heparin are not as effective as throm!olysis or angioplasty. /he

safest and most effective line of treatment would therefore !e to perform coronary angioplasty.

1*+. % &+,year,old,man presents to .asualty with a history of syncope. %n E.3 shows complete heart block. Which of the following physical signs is consistent with the diagnosis? #egular cannon JaK wa"es on Q1> ;oft first heart sound 6ow,"olume pulse ?asal systolic murmur 6oud second heart sound

our answer

.omplete heart block produces a slow regular pulse /*'2'0Fmin0 that doesnKt "ary with exercise. Usually) there is a compensatory increase in stroke "olume with a large,"olume pulse and systolic flow murmurs. .annon JaK wa"es are irregularly seen) and the intensity of the first and second heart sound "aries due to the loss of atrio"entricular synchrony.

1*B. A A0-year-old woman presents with a =-month history of fatigue# weight loss# night sweats and a degree of e"ertional dyspnoea. %er past history includes a prosthetic mitral valve replacement ;.5 years ago. She is pyre"ial with evidence of mitral regurgitation and splinter haemorrhages. )cho confirms moderate paravalvular mitral regurgitation. Dlood cultures are ta en and a diagnosis of infective endocarditis made. *hat is the most li ely infecting organism in this case+ Coxiella burnetii Enterococcus spp Staphylococcus aureus

Staphylococcus epidermidis Streptococcus viridans our answer /he commonest infective cause of native valve endocarditis in the E? is still Strep. viridans# accounting for around A0B of all cases. Enterococcus spp accounts for appro"imately 60B of cases and is more prevalent in the elderly. Staph. spp account for around ;5B of cases of endocarditis. -n the first year following prosthetic valve replacement the spectrum of infecting organisms is somewhat different# with coagulase-negative staphylococci !eing the most common (around 50B). /he ma@ority of these are Staph. epidermidis. After the first year following valvular surgery the spectrum of infecting organisms is very similar to that for native valve endocarditis.

180. A ;5-year-old man presents to the emergency department with a 6-wee history of fever and myalgia. %e had travelled to $hile ' wee s ago. 5n e"amination there are no positive findings# although the patient recollects that his right eyelid was swollen for a few wee s after he left $hile. )$7 reveals nonspecific# /-wave changes in all leads. *hat is the most li ely diagnosis+ )chinococcosis 2alciparum malaria Schistosomiasis /o"oplasmosis /rypanosomiasis our answer Trypanosoma cruzi. causes American trypanosomiasis or $hagas disease and is 0uite common in South America. /he vectors are reduvid !ugs. /he trypanosomes are transmitted !y scratching infected faeces of the !ug into s in

a!rasions caused !y the !ug during !lood suc ing. -n acute trypanosomiasis# the patient presents with fever# myalgia# hepatosplenomegaly and myocarditis. Enilateral perior!ital oedema and swelling of the eyelid can result from a !ug !ite around the eyes. /his is called 9omana,s sign. /he other conditions listed can cause myocarditis# !ut the !est choice is trypanosomiasis.

181. *hich of the following !est descri!es the mechanism of action of flecainide as an antiarrhythmic agent+ Slows the upstro e of the action potential our answer -ncreases the action-potential duration %as a direct mem!rane effect -ncreases vagal tone Affects SA and A1 nodes

2lecainide# a class -c agent slows the upstro e of the action potential and is its main mechanism of action. -t has minimal effects on action-potential duration. -n other words# it causes a mar ed decrease in conductivity# with little effect on refractoriness. /he antiarrhythmic group that mainly affects sinoatrial and atrioventricular nodes# and thus has a direct mem!rane effect# is the calciumchannel !loc ers. $lass 1 agents (digitalis agents) affect SA and A1 nodes !y increasing vagal tone.

18*. Erinary hesitancy as a sign of drug-induced to"icity is characteristic of which of the following antiarrhythmics+ Amiodarone Sotalol

Disopyramide our answer 2lecainide 1erapamil Amiodarone causes hepatic effects# peripheral neuropathy# pro"imal myopathy# thyroid dysfunction# s in discoloration and pneumonitis# among others. Sotalol (F-!loc ers) and flecainide have negative inotropy and $GS effects. 1erapamil causes !radycardia.

188. % =&,year,old man with chronic heart failure is re"iewed in terms of his drug therapy. Which of the following treatments has no pro"en mortality benefit? ?isoprolol Aigoxin Enalapril Hitrates and hydrala4ine ;pironolactone

our answer

?isoprolol /.5?5; 550) spironolactone /#%6E;0) enalapril /.:H;EH;U;0 and nitrates and hydrala4ine /1,-EF!0 ha"e all been shown to impro"e mortality in chronic heart failure. Aigoxin reduces the risk of death due to heart failure but o"erall cardio"ascular mortality is similar to that on placebo) probably reflecting a small increase in the risk of arrhythmic death with digoxin therapy.

18<. % patient with left "entricular failure undergoes echocardiography. Which is the correct formula for calculating the eIection fraction /EF0? EF R end diastolic "olume /EA10 2 end,systolic "olume /E;10FEA1 EF R end diastolic "olume /EA10 2 end,systolic "olume /E;10Fheart rate /-#0 our answer

EF R heart rate /-#0 S end diastolic "olume /EA10Fend,systolic "olume /E;10 EF R heart rate /-#0 S end,systolic "olume /E;10Fend diastolic "olume /EA10 EF R end,systolic "olume /E;10 2 end diastolic "olume /EA10FEA1 EIection fraction /EF0 is calculated using the following e$uation7 EF R /end diastolic "olume TEA1U , end,systolic "olume TE;1U0 F EA1

18'. % '',year,old man who has sustained an acute 95 subse$uently presents with heart failure. %s well as other treatments the cardiologist has recommended that abeta,blocker be commenced. %ccording to currently a"ailable e"idence which of the following beta, blockers would be most appropriate? .eliprolol 6abetalol ?isoprolol >ropranolol ;otalol

our answer

?eta,blockers may produce benefit in heart failure by blocking sympathetic acti"ity. ?isoprolol and car"edilol reduce mortality in any grade of stable heart failure. !reatment should be initiated by those experienced in the management of heart failure. %ccording to currently a"ailable e"idence /see H5.E guidelines on cardiac failure) *0080) bisoprolol) metoprolol sustained release and car"edilol ha"e shown the most useful effects. %t present metoprolol is not licensed in the UO for this indication and so car"edilol or bisoprolol are the preferred choices.

18=. % 8+,year,old man of .hinese descent who smokes =0 cigarettes per day presents to his 3>. -e is de"eloping pain at rest in his legs) and is unable to walk more than a few yards due to ischaemic pain. :n examination there is prolonged capillary refill and necrotic ulcers at the tips of his toes. !here is also e"idence of thrombophlebitis. What diagnosis fits best with this clinical picture? ?uergerKs disease ;imple peripheral "ascular disease >olyarteritis nodosa Familial hypercholesterolaemia our answer

!emporal arteritis ?uergerKs disease /thromboangiitis obliterans0 is an occlusi"e inflammatory disease of small, to medium,si4ed arteries of the upper and lower extremities. -istopathology examination of affected arteries re"eals fresh inflammatory thrombus within both small, and medium,si4ed arteries and "eins) with giant cells surrounding the thrombus. !he disease is "ery closely associated with hea"y smokingE continued smoking after diagnosis in"ariably leads to a poor outlook) gangrene and multiple amputations. >re"alence is higher in men and people of Far, Eastern origin. !he main goal of therapy is elimination of tobacco smoking. ?ypass surgery is of "ariable success due to the distal nature of the occlusions. ;ympathectomy may be useful in increasing distal blood flow and relie"ing pain. %mputation of gangrenous digits is fre$uently re$uired.

18&. % 1&,year,old youth is brought to the 3> by his mother. -e was pre"iously seen * weeks earlier suffering from acute pharyngitis. -is teeth are in generally poor condition) but otherwise there is no pre"ious medical history. :n examination he is febrile with a temperature of 8+.* V.) and has a polyarthritis affecting his knees) ankles) wrists and elbows. -e also appears to ha"e subcutaneous nodules o"er his elbows) and mitral regurgitation on cardio"ascular examination. What diagnosis fits best with this clinical picture? ?acterial endocarditis Qu"enile rheumatoid arthritis ;carlet fe"er #heumatic fe"er our answer .ongenital "al"ular heart disease !his patientKs clinical condition is highly suggesti"e of rheumatic fe"er. >hysical findings suggesti"e of rheumatic fe"er include the history of pre"ious pharyngitis) fe"er) polyarthritis) carditis /including the mitral regurgitation murmur0 and the presence of subcutaneous extensor surface nodules. 6aboratory testing suggesti"e of the diagnosis would include a positi"e anti,streptolysin : titre /peaks at <2' weeks after a streptococcal throat infection0) raised erythrocyte sedimentation rate /E;#0) .,reacti"e protein /.#>0 and a leucocytosis is also suggesti"e of rheumatic fe"er. %cute treatment includes a course of penicillin to eradicate throat carriage of group % streptococciE where there is carditis or arthritis) aspirin or prednisolone may be added) but specialist ad"ice is ad"ised. Erythromycin may be used in penicillin,allergic patients.

18+. % 80,year,old man presents complaining of whee4ing and loose motions. :n examination he has prominent precordial pulsations. What is the most likely diagnosis?

.arcinoid heart disease .ongenital tricuspid regurgitation -51,associated heart disease #heumatic heart disease !raumatic heart disease

our answer

.arcinoid heart disease occurs when there is an accumulation of fibrous tissue in the heart) especially to the undersurface of the tricuspid "al"e. 5t can hold the tricuspid "al"e in a semiclosed position) so tricuspid stenosis and regurgitation can occur. 5f it affects the pulmonary "al"e) pulmonary regurgitation or stenosis occurs. 5t is usually associated with carcinoid tumour of the bowel and with li"er metastases. ?ronchospasm) diarrhoea and flushing are part of the carcinoid syndrome. !raumatic tricuspid regurgitation can occur due to ruptured chordae tendinae) but there is no whee4ing or diarrhoea. -51 can cause cardiomyopathy) pericardial diseases) myocarditis and heart failure.

18B. % patient with an aortic "al"e replacement de"elops right hemiparesis. .! scan shows cerebral infarction. !here is no e"idence of cerebral haemorrhage. !he 5H# is *.0. -ow would you manage this case? #e"erse the anticoagulation with "itamin O ;top warfarin and start intra"enous heparin 5ncrease the dose of warfarin .ontinue warfarin and add intra"enous heparin Aecrease the dose of warfarin until the 5H# is 1.'

our answer

Use of oral anticoagulation may result in haemorrhage in the infarcted area. %s the patient has a mechanical "al"e) anticoagulation must be continued. !he best option therefore would be to stop the warfarin and start intra"enous heparin. !he reason for this is that heparin can be more easily controlled than oral anticoagulation during the acute period of stroke reco"ery.

1<0. % &0,year,old man undergoes successful A. cardio"ersion for atrial fibrillation /%F0. Which one of the following factors best predicts long,term maintenance of sinus rhythm following this procedure? %ge under &' years Hormal left "entricular function Warfarin therapy Ho alcohol intake

%F duration less than = months prior to cardio"ersion

our answer

.ardio"ersion has a much higher success rate in patients with structurally normal hearts but the left atrial si4e is a better predictor than left "entricular function. %F is likely to be persistent where the left atrial dimension is W' cm. %ge is much less important than the duration of %F. !he success of cardio"ersion drops off significantly after = months of persistent %F and long,term sinus rhythm is unlikely to be restored if %F has been persistent for more than 1* months. %lcohol is an important aetiological factor but less significant than %F duration. Warfarin is important to reduce stroke risk but does not help to restore or maintain sinus rhythm.

1<1. % =+,year,old,man with atrial fibrillation /%F0 is admitted electi"ely for A. cardio"ersion) to be performed as a day,case procedure. -owe"er) the procedure is postponed to a later date. Which one of the following reasons could be responsible for the delay? -e had discontinued digoxin for the last * days -e was taking amiodarone -is 5H# 8 weeks ago was 1.= our answer -is serum potassium le"el was <.* mE$Fl -e had an episode of angina * days ago %lthough the 5H# on the day of cardio"ersion is important) the 5H# should be optimal in the preceding 8,< weeks prior to cardio"ersion. External cardio"ersion is a safe and effecti"e method for restoring sinus rhythm) and should be attempted at least once in e"ery patient with chronic %F. :"ert congesti"e heart failure) hypokalaemia and hypothyroidism should be controlled as much as possible before cardio"ersion. %cute myocardial infarction is not a contraindication to cardio"ersion. 5f the patient has a slow "entricular response of %F in the absence of anti,arrhythmic drugs) cardio"ersion should be performed after the insertion of a temporary trans"enous,pacing catheter. Electrical cardio"ersion is initially successful in &02B<( cases) but relapse is fre$uent /*'2 '0( at 1 month and &02B0( at 1 year0. !he success depends on the duration of %F) transthoracic impedance) left atrial si4e and the age of the patient. Aigoxin should be withheld on the day of cardio"ersion. -owe"er) if digoxin toxicity is suspected) the problem should be resol"ed before cardio"ersion is attempted. >re,treatment with amiodarone or sotalol may pre"ent early recurrence. !he initial shock strength should be 100 Q) followed by a second *00,Q shock and a third 8=0,Q shock. 5f %F persists) a second 8=0,Q shock with the paddles in the anteroposterior position can be attempted. 5mmediate A. cardio"ersion) after the administration of intra"enous heparin) is appropriate in an emergency or if %F has been present for less than <+ hours. 5n electi"e cases) patients should be established on warfarin to gi"e an 5H# of between * and 8 for a minimum of three weeks prior to cardio"ersion. %nticoagulation

should be continued for four weeks after successful cardio"ersion.

1<*. A 50-year-old man presents with a 6-hour history of severe central chest pain. /here is no significant past medical history. %e is haemodynamically sta!le with pulse rate of &0 !pm and !lood pressure of 6;0(40 mm %g. )$7 shows 5 mm of S/-segment elevation in the anterior leads (1;31A). %e received aspirin =00 mg in the am!ulance and 5 mg diamorphine. *hat would !e the ne"t line of treatment+ $lopidogrel )no"aparin 7--!(--a !loc er Strepto inase /issue plasminogen activator our answer /his relatively young man has presented early with acute anterior myocardial infarction. /he ey therapeutic aim is early reperfusion in an attempt to save myocardium. -n centres with rapid access to primary angioplasty this would !e the optimum strategy. %owever# in the E? this is a rarity and far from the norm. All patients with suspected >- should receive aspirin. -n youngishH patients presenting early (within A hours) with acute anterior >-# throm!olysis with accelerated tissue plasminogen activator (t.A) should !e considered since it is associated with a small !enefit in the mortality rate over strepto inase. /he downside is the costC t.A is several times more e"pensive than strepto inase. X!he e"idence /3U;!: trial0 is for patients less than '' years of age) male) and within < hours but most would agree for patients less than =0 years of age.

1<8. A =&-year-old female is admitted with pulmonary oedema# !lood pressure ;=0(6A0 mm%g and fundoscopy showing retinal haemorrhages and papilloedema. She has systemic sclerosis and asthma. *hich of the following agents would !e the most appropriate immediate management+ -ntravenous la!etalol -ntravenous sodium nitroprusside Atenolol Gifedipine oral our answer Gifedipine su!lingual /he malignant phase of hypertension is a rare condition characterised !y very high !lood pressures# with !ilateral retinal haemorrhages and(or e"udates or cotton wool spots# without the added re0uirement for papilloedema. All patients with malignant hypertension should !e admitted for assessment# investigation# and commencement of therapy under supervision. /he initial aim of treatment is to lower the diastolic pressure to a!out 6003605 mm%g over a period of ;3= days# with oral therapy and dose escalation at daily intervals if necessary. /he ma"imum initial fall in !lood pressure should not e"ceed ;5B of the presenting value. Dlood pressure should !e measured A-hourly. /he first-line oral antihypertensive agent is either a short-acting calcium antagonist (such as nifedipine) or a !loc er (such as atenolol). Deta-!loc ers are contraindicated in asthma. An appropriate dose of nifedipine is 603;0 mg of the ta!let formulation# which can !e repeated or increased as necessary to !ring a!out gradual reduction in !lood pressure. Gifedipine is not a!sor!ed from the oral mucosa# and there have !een reports of complications including visual loss# cere!ral infarction# and myocardial infarction with nifedipine therapy using the short-acting su!lingual capsules. Su!lingual nifedipine produces unpredicta!le falls in !lood pressure and should never !e used. A$) inhi!itors and Angiotensin -- receptor antagonist are !eneficial in the treatment of renal failure in patients with scleroderma.

1<<. Which one of the following statements ?E;! describes primary pulmonary hypertension? !he familial form is inherited as sex,linked recessi"e .hronic thromboembolic disease can be identified in 80( of primary cases ;pontaneous remission is the rule in more than half the cases .annabis inhalation may induce similar disease !he risk for subacute bacterial endocarditis is low and antibiotic prophylaxis is seldom re$uired

our answer

:ne of the diagnostic criteria includes a mean pulmonary artery pressure of more than *' mm-g at rest or more than 80 mm-g with exercise. #ecurrent thromboembolism is one cause of secondary pulmonary hypertension /not primary0. Fenfluramine) cocaine inhalation and -51 infection can cause pulmonary "ascular disease with clinical and pathological features similar to those of primary pulmonary hypertension. !he familial form is inherited as autosomal dominant. !he medium period of sur"i"al is two to three years after the diagnosis. #ecent impro"ement in diagnosis and newer forms of treatment ha"e impro"ed sur"i"al) but the prognosis is generally "ery poor and most patients gradually succumb to progressi"e right,sided heart failure.

1<'. % =B,year,old man presents with an +,hour history of chest pain. E.3 shows an inferior wall infarction with ;! ele"ation of 8 mm. !here is no history of diabetes mellitus) inIury or pre"ious surgery. ?lood pressure is 18*F&0 with a pulse of '+. Which of the following treatments would be most appropriate? !issue plasminogen acti"ator %spirin ;treptokinase -eparin 9etoprolol

our answer

9any large trials ha"e shown that thrombolysis within 1* hours reduces the extent of "entricular damage and the mortality rate. !issue plasminogen acti"ator /!>%0 achie"es higher reperfusion rates but may be associated with a higher risk of stroke. !>% tends to be gi"en in preference to streptokinase in patients under '0 years of age with anterior wall myocardial infarctions where the blood pressure is low /systolic D 100 mm-g0) and in those patients who ha"e pre"iously recei"ed streptokinase. !>% is more effecti"e than streptokinase only if it is administered within < hours of the onset of chest pain. 5ntra"enous heparin may be gi"en after the initial thrombolytic therapy though its role is doubtful. %spirin /800 mg tablet0 is usually recommended. Following initiation of

thrombolysis) an intra"enous ,blocker such as metoprolol is gi"en) especially if the heart rate is W 100 beats per minute with persistent pain. 1<=. % 80,year,old woman with a pre"ious history of deep "ein thrombosis is expecting her first child. Auring which phase of her pregnancy and puerperium does she ha"e the greatest risk of "enous thrombosis? First trimester ;econd trimester !hird trimester Auring deli"ery First = weeks after deli"ery

our answer

!here is an increase in thromboembolic complications because of the hypercoagulability that exists postpartum. %nticoagulants may be necessary during pregnancy to pre"ent or control the following7 "enous thrombosis) pulmonary embolism) rheumatic mitral "al"e disease) prosthetic heart "al"es) peripartum cardiomyopathy) primary pulmonary hypertension and EisenmengerKs syndrome.

1<&. A A0-year-old man is referred !y his 7. for advice with regard to primary prevention of cardiovascular disease. %e is a smo er with a strong family history of premature death from ischaemic heart disease. 2ollowing a period of lifestyle modification# his fasting cholesterol concentration is 4.; mmol(l. 5n consultation of the local guidelines you find that his estimated 60-year ris of a coronary heart disease event is I =0B. *hat would you advise+ $holestyramine Dietician advice 2i!rate Gicotinic acid Statin our answer

/he Gational Service 2ramewor for $oronary %eart Disease (;000) and the Joint Dritish Society 7uidelines recommend targeting individuals with a 60-year ris of a coronary heart disease event of I =0B. -ndividuals should !e offered interventions to address all modifia!le ris factors# including dietary advice# smo ing cessation advice and support# moderation of alcohol consumption and weight reduction where appropriate. -n respect of lipid management# nonpharmacological and pharmacological interventions should !e utilised to achieve a total cholesterol concentration K 5.0 mmol(l and an LDL cholesterol concentration of K =.0 mmol(l. /he results of several important trials support the use of statins in primary prevention# these includeM *5S$5.S (pravastatin) A2$A.S(/)N$A.S (L)1AS/A/-G).

1<+. A 5'-year-old-woman suffers a cardiac arrest while on the ward. A rhythm strip shows 12. *hat is the strength (in @oules) recommended for the monophasic shoc used for defi!rillation+ 50 600 ;00 =00 =60 our answer /hree-0uarters of arrests are due to ventricular fi!rillation. 5nly a small proportion is due to electromechanical dissociation ()>D)# the rest !eing due to asystole. )>D usually has a potentially reversi!le causeM O O O O O hypovolaemia hypo"ia hyper alaemia hypo alaemia hypothermia

O O O O

tension pneumothora" tamponade to"icity due to drugs throm!oem!olism

Defi!rillation is used to convert 12 to sinus rhythm. .reviously the recommendation was -nitially a monophasic ;00-@oule shoc # followed !y ;00-J and then =60-J shoc s. Gew resusciation guidelines now recommend shoc ing at =60-J.

1<B. Which one of the following features is 9:;! typical of coarctation of the aorta? !he coarctation is proximal to the left subcla"ian artery origin if the right arm blood pressure is significantly higher than in the left arm .ontinuous murmur o"er the thoracic spine usually originates from extensi"e collaterals #ib notching on plain chest M,ray can be identified as early as three months after birth %trial septal defect /%;A0 is the commonest associated congenital abnormality !he risk for subacute bacterial endocarditis is low and antibiotic prophylaxis is seldom re$uired our answer

!he commonest site of discrete obstruction of the aortic lumen is Iust distal to the origin of the left subcla"ian artery. !he systolic arterial pressure in the arms exceeds that in the leg. 5f the systolic arterial pressure in the right arm is higher than that of the left arm by more than 80 mm-g) the left subcla"ian is in"ol"ed in the coarctation. .ontinuous murmur o"er the thoracic spine usually originate from small) tight coarctation /D * mm0. :ther cardiac malformations are fre$uent) the commonest being a bicuspid aortic "al"e. Hotching of the inferior border of the ribs from collateral "essels is common and usually manifest in adults and older children. >atients with coarctation are at high risk of subacute bacterial endocarditis and should be strongly ad"ised about antibiotic prophylaxis.

1'0. % 8+,year,old man presents for re"iew. -is only pre"ious history of note has been recurrent shoulder subluxation. -is main complaints are tiredness and increasing dyspnoea

on exertion. !he nursing clerking on admission notes that he seems "ery tall and thin) his height is described as 1.B8 m /=ft < inches0. :n examination his blood pressure is 1='F&0 mm-g) he has left "entricular hypertrophy) a low,pitched apical diastolic murmur and an early systolic apical eIection murmur. What diagnosis fits best with this clinical picture? 9itral stenosis %ortic regurgitation our answer 9itral "al"e prolapse %ortic stenosis 5nfecti"e endocarditis !his man has a marfanoid habitus and is at risk of suffering aortic regurgitation. %etiological factors in"ol"ed in aortic regurgitation include infecti"e endocarditis) rheumatic heart disease) trauma with "al"ular rupture) congenital bicuspid aortic "al"e) myxomatous degeneration) syphilitic aortitis) systemic lupus erythematosus /;6E0) aortic dissection and the use of amphetamine slimming products. ;ymptoms of aortic regurgitation include dyspnoea on exertion) syncope) chest pain and congesti"e heart failure. .ardiac auscultation characteristically re"eals displacement of the cardiac impulse downwards and to the left) prominent ;8 heard o"er the apex) a low,pitched apical diastolic rumble /%ustin2Flint murmur0 and an early systolic apical eIection murmur. .hest M,ray may re"eal left "entricular hypertrophy and aortic dilatation. Echocardiography re"eals the coarse diastolic fluttering of the anterior mitral "al"e leaflet. ;urgical "al"e replacement is indicated in symptomatic patients with chronic aortic regurgitation who ha"e symptoms despite optimal medical management) and in acute aortic regurgitation where there is e"idence of left "entricular failure. 5deally) surgery should be considered before the eIection fraction falls to below ''(.