Aortic stenosis

ECG: Sinus rhythm; left atrial enlargement (wave duration P > 110 ms, bifid in leads I, II, V6, wide terminal component in V1); systolic left ventricular hypertrophy (Sokolow index of 37); widened QRS (115 ms) with incomplete left bundle branch block pattern; lateral repolarization disorders;

Comments: Aortic stenosis is the most common acquired valve disease. It is a disease of the elderly, especially common after age 65 with a clear male preponderance. Aortic stenosis is defined as an obstruction of left ventricular ejection most often located at the level of the aortic valve. The impediment to left ventricular ejection results in increased afterload and left ventricular pressure. The rise in left ventricular wall strain induces concentric myocardial hypertrophy without cavity dilatation which, initially, allows maintaining normal overall ventricular systolic performance and satisfactory downstream flow. After several years, the hypertrophied myocardium loses part of its contractile properties, with the failure of the compensation mechanisms leading to a decrease in the overall systolic performance of the ventricle and to a clinical picture of heart failure. Wall hypertrophy can lead to functional myocardial ischemia in the absence of any coronary lesion by loss of the vasodilatory response of intramyocardial arterioles and increased oxygen requirements. Due to thickening of the wall, the diastolic properties of the left ventricle are also altered with compliance disorder, slowed relaxation and increased filling pressures. Atrial contraction plays a predominant role in ventricular filling, which explains the hemodynamic alteration observed during the loss of sinus rhythm and a passage in atrial fibrillation. The overload of the left atrium is much more discreet than that of the left ventricle and there is no overload of the right cavities until a very late stage of heart failure. Conduction disorders are frequent and can be caused by left intraventricular hypertension and extension of interventricular septal calcifications (contiguity of the aortic sigmoid valves and of the bundle of His and its branches). The electrocardiographic expression observed in aortic stenosis can be deduced from these pathophysiological data with predominant signs of left ventricular hypertrophy but also possible alterations in P wave pattern, signs of myocardial ischemia and conduction disorders.

• The electrocardiogram can remain normal even in some patients with severe aortic stenosis (about 20% of cases);
• Left ventricular hypertrophy with systolic overload is common; it results in the presence of an R wave of increased amplitude in left precordial leads (amplitude generally less than for aortic insufficiency), with moderate delayed intrinsicoïd deflection, disappearance of the q wave, possible moderate ST segment depression and T wave inversion and by the presence of a deep S wave in right precordial leads; this hypertrophy may lack or vary from a simple moderate increase in voltages to a caricatural pattern; the signs of hypertrophy are proportional to the degree of obstruction and the increase in electrical patterns on successive tracings are indicative of the progression of the aortic stenosis;
• The QRS axis may be normal or deviated to the left;
• The P wave can long maintain a normal pattern in the absence of associated mitral valve disease; there may be relatively discrete signs of left atrial enlargement (indirect reflection of obstructed left ventricular ejection), which relate more to the marked terminal negativity of the P wave in V1 than to the duration of the P wave, slightly prolonged as a rule, or to bifid morphology; atrial fibrillation is observed in about only 10% of patients, mostly in elderly patients and in severe and advanced forms;
• Electrical signs of functional coronary insufficiency are possible but should be investigated for associated coronary artery disease; these may reflect primary alterations in repolarization; in practice, it is difficult to differentiate between repolarization abnormalities directly related to left ventricular hypertrophy and those possibly related to myocardial ischemia; coronary artery disease is suspected when the inversions are particularly deep, symmetrical and peaked or when present in the inferior or right precordial leads and not only in lateral leads;
• Intraventricular and atrioventricular conduction disorders may be observed; an incomplete bundle branch block is by far the most common conduction disorder and is most often the result of mechanical crushing and retraction phenomena of the left branch network in the middle or upper portion of the septum (increased intraventricular pressure, modified kinetics of the hypertrophied myocardium); the other conduction disorders (complete left bundle branch block, right bundle branch block, atrioventricular blocks) are the direct result of the aortic valvular and juxtavalvular calcifications which compress or sever the terminal portion of the bundle of His and its bifurcation; it should be noted that the presence of a conduction disorder (left block, atrioventricular block) may mask the pattern of left ventricular hypertrophy;
• After aortic valve replacement surgery, a progressive regression of the signs of left ventricular hypertrophy is common albeit inconstant and variable in its intensity and swiftness; the conduction disorders are generally non-regressive and on the contrary can complicate surgical outcomes (frequent postoperative atrioventricular blocks);

Take-home message: Systolic left ventricular hypertrophy is the most characteristic electrical sign of aortic stenosis.