Biomedical subjects
Publications and source records attributed to E Dupasquier.
This case report describes an unrecognized adverse effect of an ACE inhibitor (enalapril): attack of acute abdominal pain. This symptom was observed 3 times over a period of 5 years in a 43 year old woman, occurring 24 h after she was taking the ACE inhibitor, and disappearing 3 to 5 days after the withdrawal of enalapril.
On the occasion of three cases of primary hyperaldosteronism the author expresses disapproval of the recently published recommendation of a general screening for aldosterone, plasma renin activity and their respective quotient in all hypertensive patients. Compared with the rareness of the disease, this screening seems extremely expensive and mostly useless. Even in view of the possibility of delaying diagnosis of extremely rare cases of normokalemic primary hyperaldosteronism by three to five years--an occurrence without negative consequences--the author recommends as a first step to follow clinical parameters by repeated determination of potassium and to engage highly specific and expensive tests not before strong suspicion for hyperaldosteronism arises. In 1994 costs of public medicine have increased to intolerable levels; therefore the consideration of a price/quality ratio is mandatory.
The authors reports an unrecognised secondary effect, but perhaps not as rare as has been thought, of enalapril: the acute abdomen. Three similar cases have previously been reported. The underlying mechanism is probably the inhibition of degradation of tissue kinins to inactive peptides as in subcutaneous and/or submucous angioneurotic oedema. Todate, this secondary effect has not been reported with other angiotensin converting enzyme inhibitors. The relationship between the acute abdomen and angioneurotic oedema with primary hyperaldosteronism is discussed.
The chronological relationship between the S2 of the phonocardiogram and the T wave of the ECG, and the behaviour of the QT and QTc intervals, have been investigated in two cases of idiopathic long QT syndrome (LQTS) at rest and during effort. At rest and during effort with heart rates (HR) under 120/min, the S2 is always abnormal before the end of the T wave where the QTc interval is generally prolonged, but is sometimes within normal range (less than or equal to 440 msec). In cases where the QTc interval falls within normal range, the use of Bazett's formula to calculate the QTc interval may mislead and cause the existence of LQTS to be overlooked. Study of the chronological relationship (timing) between S2 and T wave is a reliable method of detecting LQTS even with a normal QTc interval. During ergometer exercise, if we observe (as in our two cases) not only a normal acceleration of the HR but a shortening and even a normalization of the QTc interval, therapeutic abstention (betablockers) may be recommended in asymptomatic LQTS. It is concluded that (1) in LQTS at rest and with HR under 120/min, S2 is always abnormal before the end of the T wave, (2) study of the timing S2/T wave is a reliable method of detecting the existence of LQTS even with a normal QTc interval, (3) in asymptomatic LQTS where the QTc interval shortens or falls within normal range during effort with S2 appearing at the end of the T wave, as reported in our first case, therapeutic abstention (betablockers) may be recommended.
Chest pain due to esophageal spasm or esophagitis may mimic pain of variant angina. Differential diagnosis of the two diseases is often difficult and requires various tests, the value of which is discussed. These problems are illustrated by three cases. The esophageal investigation should preferably be preceded by coronary arteriography. Chest pain or dysphagia due to iced drinks is not specific for esophageal spasm but may be due to coronary spasm.
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Mitral valve prolapse syndrome is the most widespread cardiac disease (3-8% of subjects presumed healthy) but the auscultatory findings are still too little known and may often cause misunderstanding. Although the prognosis is generally excellent, it may in rare cases be complicated by infective endocarditis, severe mitral regurgitation, rupture of chordae tendineae, severe arrhythmias which may be the cause of sudden death and recurrent transient cerebral ischemic attacks. These last two rare complications are illustrated by two clinical cases, and the pathogenesis and therapy are discussed.
In the light of 4 personal observations of PPPRINZMETAL's angina, a review has been conducted of the literature in the 15 years since the condition was first described. Although the formal diagnostic criteria for this form of angina simultaneously clinical, biological and electrical - anginal attacks occurring at rest, often at night, during which elevation of the ST segment is recorded which disappears at the end of the attack without any significant rise in enzyme levels (SGOT and CPK) - the frontiers of the syndrome appear to have widened since PRINZMETAL's description: - Severe proximal stenosis of the coronary arteries is not obligatory; they may be only slightly damaged or even healthy. - Prinzmetal's angina is by no means always "spontaneous" but is often induced, either by psychic factors, which explain the fixed time of the attacks, or by organic factors, e.g. cold drinks (Observation No.2). In this event it would appear safer to speak of angina or rest as opposed to angina of effort. - In contrast to what PRINZMETAL thought, effort tests may sometimes induce angina-type pain with elevation of the ST segment, and here the borderline between this syndrome and conventional angina with ST segment elevation after effort test (5% of cases) is less clear-cut. The two nosologic entities probably reflect the same physiopathological situation, i.e. acute myocardial ischemia, and may represent the same affection in different phases of development. The prognosis is equally bad. - Attacks of rinzmetal's angina are often accompanied by severe and sometimes fatal disorders of rhythm, and this influences the therapeutic approach. - The coronary spasm posited by PRINZMETAL and others before the advent of coronarography is indeed, in the majority of cases, the immediate cause of myocardial ischemia and anginal pain, without any preliminary increase in the energy requirements of the heart as in the conventional anginal attack. - A vasoactive substance present in the circulating blood at the beginning of the affection, which may be degraded and subsequently disappear and may be secreted by the pathologic coronary artery, was demonstrated in observation No. 4: this may, in conjunction with vagal hypertonia, be the causative factor in coronary spasm. Study of its pharmacodynamic properties is now in progress.
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