Valvular Heart Disease

Trans-thoracic and trans-esophageal echo and coronary angiography before open heart surgery are the investigations used. CT chest is not one of them; only a CT aortogram is used, in patients with aortic aneurysm.

The murmur of aortic regurgitation is a soft blowing decrescendo (diastolic) murmur best heard at the second aortic area. MR gives a holosystolic murmur on the apex, and the aortic stenosis murmur is propagated to the neck and to the apex.

The apex is sustained (heaving) in left ventricular hypertrophy and hyperdynamic in dilatation; aortic stenosis gives signs of left ventricular hypertrophy with a sustained apex. Aortic regurgitation gives a hyperdynamic apex.

A palpable diastolic thrill at the apex is a sign of mitral stenosis. MR gives a palpable systolic thrill at the apex, and aortic stenosis a systolic thrill at the first aortic area.

Surgical aortic valve replacement is indicated in severe aortic stenosis and in severe aortic regurgitation. Mild and moderate aortic lesions are not indications.

Aortic valve replacement (SAVR or TAVR) is indicated in severe aortic stenosis. The other options are mitral lesions.

Mitral valve intervention (PBMV or surgical replacement) is indicated when the mitral valve area is < 1.5 cm2, and severe MS is an area < 1 cm2. The other options are aortic lesions.

A metallic (mechanical) prosthesis needs warfarin for life with INR 2.5-3.5, so (a) is false. Lifelong warfarin brings a bleeding risk, and the valve carries a clot risk, while its durability is long.

A bio prosthesis needs warfarin for 3-6 months, then antiplatelet therapy, so long-term warfarin is not needed. Its durability is short and its risks of thromboembolism and bleeding are low.

Surgical aortic valve replacement is indicated in severe aortic regurgitation. Mild or moderate aortic stenosis and mitral lesions are not indications.

A mechanical valve is durable, so 'decreased durability' is false. It needs warfarin for life, which brings its clot and bleeding risks; durability is inferred from the line 'If metallic prosthesis: warfarin for life', as the handout does not state it.

A bio prosthesis needs warfarin for 3-6 months, then antiplatelet therapy, not long-term anticoagulation. It is less durable and has less risk of thromboembolism and bleeding.

Intervention or surgery is indicated in severe MR, symptomatic or asymptomatic with EF < 60% and/or a dilated LV. Moderate MR is not an indication, and aortic stenosis is treated on the aortic valve.

Mitral valve intervention is indicated in MS with a valve area < 1.5 cm2 and in severe MR. Mild lesions and moderate MR are not indications.

Average survival in symptomatic aortic stenosis is 2 years with heart failure, 3 years with syncope and 5 years with chest pain, so heart failure has the worst prognosis.

Aortic valve replacement is indicated in severe aortic stenosis and severe aortic regurgitation. In every other option the aortic lesion is mild.

Percutaneous balloon valvuloplasty is the intervention for mitral stenosis, not regurgitation. MR is treated by surgical repair or by replacement with a bio or metallic prosthesis.

Transcatheter aortic valve replacement is a treatment of severe aortic stenosis, not of the mitral valve. Mitral stenosis is treated by PBMV or surgical mitral valve replacement.

A systolic murmur at the base (first aortic area) is the murmur of aortic stenosis. The ECG in aortic stenosis shows left ventricular hypertrophy.

Prominent main pulmonary arteries and an enlarged left atrium on chest X-ray are findings of mitral stenosis. Mitral stenosis leads to pulmonary hypertension with right ventricular strain, which fits the right-sided ECG signs; AS, AR and low EF load the left ventricle.

Congenital heart disease and infective endocarditis are listed causes of tricuspid regurgitation. Inferior wall infarction is not named; it is inferred from the cause 'Functional (RV dilatation...)', as an infarction reaching the right ventricle dilates it.

The murmur of aortic regurgitation is diastolic. MR gives a holosystolic murmur and AS a systolic murmur; VSD and PS also give systolic murmurs.

Pulmonary congestion in mitral stenosis is controlled with diuretics and beta-blockers, which slow the heart rate and increase the diastolic time; diltiazem also slows the rate. A nitrate lowers the filling pressure while the narrow valve fixes the output, so it can cause marked hypotension.

Acute MR presents with bilateral coarse crepitations of acute pulmonary edema. Bedside echo shows no left ventricular dilatation, so the apex is not shifted; marked lower limb edema belongs to right sided heart failure in chronic disease.

Tricuspid stenosis gives a giant a wave and slow y descent in the JVP; the a wave comes with atrial contraction at the end of diastole, so the liver pulsation is diastolic. This is inferred from the line 'Giant a wave and slow y descent in JVP'; systolic expansion of neck veins and a pulsatile liver belong to tricuspid regurgitation.

In compensated aortic stenosis the left ventricle hypertrophies without dilating, so the apex is sustained but localized and not shifted. The handout says the aortic stenosis murmur is propagated to the neck and to the apex, and a carotid (neck) thrill could be felt. A shifted apex down and out means dilatation, which comes only after failure of compensation.

Acute severe MR presents with tachycardia, hypotension and bilateral coarse crepitations of acute pulmonary edema. There is no left ventricular dilatation, so no cardiomegaly, and marked lower limb edema is a sign of right sided heart failure.

Thickening, fibrosis and restricted mobility of the leaflets mean primary MR (structural damage of the leaflets), not secondary MR, which has no structural problem with the valve. Pulmonary and systemic congestion together mean left plus right sided failure, 'Lt. to Rt. = CHF'.

Rheumatic fever causes primary MR mostly combined with mitral stenosis, and rheumatic mitral stenosis is more common in females. Dilated and ischemic cardiomyopathy give secondary MR with no structural problem of the valve.

As left atrial pressure remains elevated the left atrium increases in size, with a greater chance of atrial fibrillation. A dilated left atrium > 50 mm is itself an indication for oral anticoagulation.

Mild MS is a mitral valve area > 1.5 cm2, moderate 1-1.5 cm2 and severe < 1 cm2; the normal area is 4-6 cm2.

A diastolic rumbling murmur on the apex with an accentuated P2 means mitral stenosis with pulmonary hypertension. Rheumatic fever is the most common cause of mitral stenosis.

An apex shifted down and outward with a palpable systolic thrill and an apical systolic murmur means MR with signs of LV dilatation, and the apex is hyperdynamic. A sustained apex is the sign of left ventricular hypertrophy in aortic stenosis.

The patient has mitral and tricuspid regurgitation with no aortic lesion, so aortic valve replacement has no place. Coronary angiography before open heart surgery, mitral valve replacement and tricuspid valve repair are all options.

Mitral stenosis gives an accentuated 1st heart sound and a diastolic rumbling murmur on the apex. A systolic murmur at the aortic area is aortic stenosis and a continuous machinery murmur is PDA.

In mitral stenosis the dilated left atrium gives a greater chance of AF, and embolic stroke could occur secondary to AF, resulting in hemiplegia. She was not taking the anticoagulation that AF requires.

Severe MS is a mitral valve area < 1 cm2 on echocardiography.

Infective endocarditis is not common in MS because of marked fibrosis and low pressure. Pulmonary hypertension, atrial fibrillation and stroke are the usual complications.

In severe mitral stenosis the left atrial pressure is high, so the valve opens early and the opening snap comes soon after S2, not late; this is inferred from that line, as the handout does not give the timing of the snap. AF and pulmonary congestion and a pulsatile liver from associated tricuspid regurgitation all fit severe MS.

Chronic AR gives a wide pulse pressure with increased systolic and decreased diastolic pressure. The left ventricular preload increases and the ventricle dilates.

Obstruction to left ventricular inflow is mitral stenosis, and rheumatic fever is its most common cause. Degenerative annular calcification and congenital causes are uncommon causes.

Mitral stenosis causes an increase in left atrial pressure, while the cardiac output decreases as it progresses.

Ankylosing spondylitis is an inflammatory cause of primary aortic root disease (annular dilatation), which causes aortic regurgitation.

The raised left atrial pressure is transmitted to the pulmonary vasculature, and long standing passive pulmonary hypertension leads to pulmonary arteriolar vasoconstriction. Edema in the walls of the small vessels is inferred from the pulmonary congestion of mitral stenosis, as the handout does not state it.

Carcinoid syndrome is listed among the causes of tricuspid regurgitation; it is not named as a cause of the other lesions.

Echocardiography, trans-thoracic and trans-esophageal, assesses the valve lesion, and coronary angiography is done in patients with suspected ischemic heart disease before open heart surgery. So all the above are used.

A localized apex directed outwards and downwards is a sign of left ventricular enlargement, while right ventricular enlargement gives a diffuse apex, so aortic stenosis is the only left-sided lesion offered. In aortic stenosis itself the handout gives the apex as localized and not shifted.

In severe AR, symptoms, LVEF < 50% and open heart surgery for other cause (CABG) are each an indication for valve replacement. LV dilatation counts only when the systolic diameter is > 50 mm, so 'dilated LV dimensions' with no size given is the weakest choice.

Congenital heart disease, infective endocarditis and rheumatic fever are listed causes of tricuspid regurgitation. Inferior wall MI is the only option not named in that list, so it is the expected answer.