A Pesola

Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina.

To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.

Contribution of recirculation and fat diffusion to myocardial washout curves obtained by external counting in man. Stochastic versus monoexponential analysis.

133Xenon and 125I-iodoantipyrine (IAP) solutions were simultaneously injected into the left coronary artery in four normal patients and four patients with coronary artery obstructions. Recirculation was computed by convolution of the fractional decrease of the curve following inlet injection over a second curve obtained following right atrial injection. Uncorrected xenon and IAP curves were not statistically different in spite of the lower myocardium-blood partition coefficient and the recirculation of xenon. Corrected IAP curves could be followed down to 1.7%, whereas xenon curves could be followed only to 7.5%, indicating significant xenon diffusion holdup in fat. Corrected IAP curves deviated from a monoexponential course below 5% of peak in normal patients and at about 10% in patients with coronary artery obstructions. Stochastic analysis gave flow values 22% lower and 45% higher, respectively, than those computed from monoexponential extrapolation of corrected IAP and uncorrected xenon curves. With the double-injection technique, IAP washout can be calculated down to about 1% of peak, accounting for the distribution of 99% of the flow through the tissue to which the indicator is delivered. Monoexponential analysis of corrected IAP curves overestimates flow, because it cannot fit the initial delay component and the final reduction of slope. Xenon washout does not allow quantification of myocardial flow in man.

Systemic and coronary haemodynamic effects of the new hypotensive drug L 6150.

The acute systemic and coronary haemodynamic effects of a new hypotensive drug L 6150 (3-hydrazino-6-[N,N-bis(2-hydroxyethyl)amino]pyridazine) have been studied in six patients with renal or essential hypertension. The drug, administered intravenously at a dose of 2-9 mg, caused a marked hypotension and increase of cardiac output in five cases. Though left ventricular work was reduced or unchanged after the drug, myocardial blood flow increased markedly, coronary resistance decreased and coronary A-V oxygen difference decreased by about 50% indicating coronary vasodilation. When compared with the available data on the effects of hydrazinophthalazine, L 6150 appeared to have qualitatively similar effects, but a somewhat greater direct coronary vasodilator effect.

Studies of Regional Myocardial Perfusion in the Anginal Patient

The pathogenesis of angina pectoris is currently related to a localized, acute imbalance between myocardial metabolic demands and coronary blood supply. An impairment of blood supply may be related: 1) to the presence of coronary artery obstruction which prevents the required increase of perfusion to meet increased myocardial demands; 2) to a sudden reduction of regional myocardial blood supply.