[Calcium antagonists in cardiology: 10 years later. I - Principles and drugs].
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Biomedical subjects
Publications and source records attributed to R Gourgon.
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The authors report 3 cases of post-infarction left ventricular aneurysm with localised rupture into the pericardium. The patients (3 men aged 54, 58 and 67 years old) had left ventricular aneurysms (2 anterior, I posterior) which ruptured early, between the second and tenth week. All presented with cardiogenic shock. The diagnosis was made by 2D echocardiography (I case) or by pericardial aspiration and angiography (2 cases). Good results were obtained by surgical evacuation of the hemopericardium and resection of the ventricular aneurysm with a follow-up of 3 to 12 months. The rarity of these cases is underlined: only three other similar cases appear to have been previously reported.
The purpose of this work was to study interactions between physical properties of the arterial system and left ventricular performance during aging in normal and in hypertensive patients. 50 patients were studied; 28 normal patients (age range 22 to 68 years) and 22 patients with essential hypertension (age range 23 to 63 years). In hypertensive patients, the end systolic pressure-volume ratio (ESP/ESV), modulus of chamber stiffness (kp), left ventricular wall thickness (h), mass (m), m/LVEDV ratio (LVEDV: left ventricular end diastolic volume), systemic arterial resistance (SAR), pulse wave velocity (C) and characteristic impedance of the ascending aorta (Zc) were increased compared to normal subjects of similar age. The ejection fraction (EF), the mean velocity of fiber shortening (VCF) and dp/dt max were unchanged. In normal patients: the ESP/ESV ratio, kp, h, m, m/LVEDV ratio, SAR, C and Zc increased with age; there were no age related changes in EF, VCF or dp/dt max. In both groups, there was a close relationship between the m/LVEDV ratio and Zc, the characteristic impedance of the ascending aorta. These results suggest that: 1. aging and arterial hypertension lead to similar changes in the physical properties of the arterial system and in left ventricular performance; 2. in both cases, the development of concentric cardiac hypertrophy is closely related to the physical properties of the arterial system.
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Verapamil inhibits calcium influx through the slow calcium canals. The coronary an haemodynamic effects of intravenous Verapamil were studied in 8 patients with chronic coronary insufficiency documented by coronary arteriography. The following measurements were made in spontaneous rhythm and during atrial pacing under basal conditions and 10 minutes after intravenous Verapamil (0.10 to 0.17 mg/kg) relayed with a continuous infusion of 5 x 10(-3) mg/Kg/mn: heart rate, cardiac output, left ventricularr pressure (Millar 5 F micromanometer), femoral artery pressure, coronary sinus flow by continuous thermodilution, oxygen and lactate concentrations in arterial and arterio-venous oxygen difference, and index of myocardial oxygen consumption and the coefficient of lactate extraction were then calculated. The coronary and haemodynamic effects of atrial pacing were similar before and after Verapamil at a given rate. Left ventricula end diastolic pressure decreased, cardiac output and total systemic resistance were unchanged, dP/dt max increased but to a lesser degree after Verapamil (P less than 0.05). Coronary arterio-venous oxygen difference decreased after Verapamil. The coronary and haemodynamic effects of Verapamil were similar in spontaneous rhythm and during atrial pacing. In spontaneous rhythm, the heart rate and left ventricular end diastolic pressure increased. In spontaneous and paced rhythm, femoral artery pressure, total systemic resistance and dP/dt max decreased. Cardiac output remained the same. Myocardial oxygen consumption decreased mainly because of a reduced coronary arterio-venous oxygen difference and because of unchanged coronary flow in spontaneous rhythm oxygen consumption seems to have a favourable effect on the myocardial energy equilibrium as shown by the increased coefficient of lactate extraction during atrial pacing after Verapamil. This study shows the negative inotropic and arterial vasodilator effects of Verapamil to be responsible for the reduced myocardial oxygen consumption. It also caused coronary artery vasodilation.
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Alkalosis was used for stress testing for coronary artery spasm in 70 patients (average age: 56 years) with resting angina. A rapid intravenous infusion of an alkaline buffer (THAM) immediately followed by 5 minutes' maximal ventilation increased the arterial pH to 7.67 +/- 0.5. Anginal pain and ECG changes were observed in 24 Patients, with ST elevation in 10 cases and ST depression in 14 cases. The ischaemic changes occurred during hyperventilation in 16 cases and in the 3 minutes following the test in 8 cases. The heart rate increased from 66 +/- II to 71 +/- 14 bpm (p less than 0,01) but systolic blood pressure fell from 139 +/- 12 to 130 +/- 12 mm Hg during hyperventilation; there was no significant change in the rate-pressure product (1130 +/- 1750 to 8990 +/- 2690). In all cases, the angina and ischaemic changes regressed after intravenous Trinitrin. Coronary angiography was performed in 56 patients: in the 24 patients with positive responses (Group I) and in 30 of the 46 patients with negative responses (Group II). Significant coronary artery narrowing (greater than 70%) was observed in 21 patients of Group I: in the 3 patients without coronary lesions an intravenous injection of 0.4 mg methylergometrine provoked coronary spasm. In Group II, significant narrowing was demonstrated in 18 patients: in the 12 other patients, coronary spasm could not be induced by methylergometrine. Therefore, in the absence of organic coronary lesions, an excellent correlation has been shown between the alkalosis and methylergometrine tests. This stress test was repeated in 16 of the 24 patients in Group I one hour after administration of 20 mg of Nifedepine: the test was negative in all cases. We conclude that the alkalosis test could be useful in the coronary care unit as a stress test for coronary spasm to determine the antianginal treatment of choice and to evaluate its efficacity.
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