[Hemodynamic and coronary effects of methylergometrin]. / Effets hémodynamiques et coronaires de la méthylergométrine.

The methylergometrine test (ME) was performed during coronary angiography in 43 patients either by a single injection of 0,4 mg (34 cases) or by fractioned doses every 5 minutes of 0,1 mg, 0,2 mg, 0,3 mg, 0,4 mg (total 1 mg) (9 cases). Opacification of the coronary arteries was performed 1, 3 and 5 minutes after each injection; left ventricular pressures were recorded with a Millar catheter-tip transducer. The heart rate and first derivative of left ventricular pressure did not vary significantly after the 0,4 mg single dose ME. Left ventricular end systolic pressure rose by 11 p. 100 (p less than 0,001) and left ventricular end diastolic pressure from 18,3 to 23,1 mmHg (p less than 0,001). Myocardial oxygen consumption assessed by the TTI rose from 2873 +/- 896 to 3083 +/- 788 mmHg.s-1 .min (p less than 0,01), but myocardial contractility as assessed by the V max fell from 1,68 +/- 0,40 to 1,58 +/- 0,35 s-1 (p less than 0,001). The reduction in the calibre of the coronary lumen was identical after the single 0,4 mg dose and the 1 mg fractioned doses. In the later case, 50 p. 100 of the maximal response was observed after the first injection of 0,1 mg. After the single dose of 0,4 g ME the reduction in coronary lumen was very rapid over the first 3 minutes. Prolonged observation up to the 10th minute (7 patients) showed slight aggravation of the vasoconstriction between the 5th and 10th minutes, justifying an injection of a nitrate derivative before discontinuing surveillance. The vasoconstriction induced by ME seems to be within the physiological limits of vasoconstriction. The maximal overall decrease of the coronary diameter was 12,3 +/- 7,8 p. 100 and never exceeded 20 p. 100. There was a significant difference in the response of atheromatous patients in whom the vasoconstriction was greater in the presence of resting angina than in the absence of resting angina (16,4 +/- 8,7 p. 100 compared to 9,7 +/- 6,4 p. 100, p less than 0,01).

[Coronary artery dilatation induced by isosorbide dinitrate injection (author's transl)]. / Action coronarodilatatrice de l'isosorbide dinitrate injectable.

Twenty-six patients were given 3 mg isosorbide dinitrate either by direct intra-coronary injection (17 patients) or by intravenous injection ( patients), 5 minutes after an injection of 0.4 mg methylergometrine. In all 26 patients isosorbide dinitrate dilated the coronary arteries to a diameter that was 26% greater than the smallest diameter observed with methylergometrine and 14.8% greater than the basal diameter. The response was highly significant at 30 seconds, maximal at 2 minutes and lasted more than 10 minutes. At the dosage level used in this study, there was no significant difference between the two groups of patients. However, a rapid fall in systemic arterial pressure was noted after peripheral intravenous injection.

Frequency of provoked coronary arterial spasm in 1089 consecutive patients undergoing coronary arteriography.

We established the incidence of coronary artery spasm provoked by 0.4 mg of methergine in 1089 consecutive patients undergoing coronary angiography. The test was performed after routine coronary arteriography. Subjects included patients with angina, both typical and atypical, patients who had recently had myocardial infarction and patients with either valvular disease or congestive cardiomyopathy. Patients with spontaneous spasm, left main narrowing or severe three-vessel disease were excluded. One hundred thirty-four patients experienced focal spasm. Focal spasm was uncommon in patients with atypical precordial pain (1.2%), angina of effort (4.3%), valvular disease (1.95%) or cardiomyopathy (0%). It occurred most often in patients with angina at rest and less often in patients with angina both at rest and induced by exercise. Spasm was provoked in 20% of patients with recent transmural infarction, but in only 6.2% of patients studied later after infarction. Spasm was superimposed on fixed atherosclerotic lesions in 60% of the patients. No serious complications were encountered. Although the patients who underwent provocation tests in this study are not representative of all patients with coronary artery disease, spasm occurred in 20% of patients who experienced a coronary event and in 15% of patients who complained of chest pain.

[Hemodynamic and coronary effects of isosorbide dinitrate: comparison of intravenous and intracoronary injection]. / Effets hémodynamiques et coronaires du dinitrate d'isosorbide: comparaison entre les voies d'injection intracoronaire et intraveineuse.

The hemodynamic and coronary effects of a single dose of 3 mg of isosorbide dinitrate (ISD) were studied in 26 patients after intra-coronary (17 cases) and intravenous injection (9 cases). The study was carried out after opacification of the coronary arteries and a 0,4 mg ergometrine test. The radiological contrast and ergometrine increased left ventricular end diastolic (10,4 +/- 0,89 mm Hg to 22,5 +/- 1,88 mm Hg) and systolic pressures (131,4 +/- 4,8 mm Hg to 158,7 +/- 5,8 mm Hg) without changing V max. After ergometrine, the diameter of the coronary vessels decreased by 8,8%. After ISD, these pressures fell significantly from the 10th second; the lowest pressure after ISD was related to the initial pressure at the end of the ergometrine test (systolic pressure Y = 0,68 X + 6,39, R = 0,89, p less than 0,001) ( end diastolic pressure : Y = 0,36 X + 0,17, R = 0,68 , p less than 0,01). Moderate transient tachycardia was probably a reflex reaction. The increase in V max, maximal after 1 to 2 minutes, seemed to have a different mechanism. The global effect is to decrease myocardial oxygen consumption as reflected by the fall in the tension - time - index (3083 +/- 2,13 to 2330 +/- 184 mm Hg . sec-1 . min . The diameter of the coronary vessels rose by 26% with respect to the smallest diameter observed after ergometrine. The intracoronary and intrafemoral venous injection gave identical hemodynamic and coronary changes from the first minute. The effects were maximal between 2 and 4 minutes and continued after 10 minutes. The only difference was a more rapid decrease in systolic pressure after intrafemoral administration. Dilatation occurred before the hemodynamic effects after intracoronary injection, which is an argument for using intracoronary ISD in the treatment of spasm induced by ergometrine.

Coronary sinus blood flow at rest and during isometric exercise in patients with aortic valve disease. Mechanism of angina pectoris in presence of normal coronary arteries.

In 46 patients with aortic valve disease, coronary sinus blood flow was measured using a continuous thermodilution method both at rest and during isometric handgrip exercise. All patients had normal coronary angiograms. The patients were separated into three groups: Group I, 12 patients with aortic stenosis (systolic gradient 72 +/- 12 mm Hg); Group II, 15 patients with both aortic stenosis and regurgitation; Group III, 19 patients with aortic regurgitation. At rest, the coronary sinus blood flow was two to three times normal. However, when corrected for left ventricular mass (ml/100 g), flow was within normal limits. The ratio diastolic pressure-time index/systolic pressure-time index (DPTI/SPTI) was decreased in all three groups at rest. During isometric exercise, coronary sinus blood flow increased significantly: by 60 percent in Group I, by 88 percent in Group II and by 118 percent in Group III. There was a significant reduction of the DPTI/SPTI ratio. Of the 18 patients with angina on effort during the test, 7 were in Group I, 6 in Group II and 5 in Group III. There were no differences in the coronary sinus blood flow between the patients with angina and those who were pain-free, either at rest or during exercise. Angina pectoris does not appear to be caused by a failure of coronary blood flow to increase. There was no discrepancy between myocardial demand, as measured by the pressure-time index and coronary blood flow. However, the DPTI/SPTI ratio was significantly lower during exercise in the patients with angina than in those who were pain-free. Underperfusion of the subendocardial muscle seems to be a causative factor in the patients with angina.