Physiologic--angiographic correlates of coronary arterial stenoses in resting and intensely vasodilated states.

The treatment of ischemic heart disease is dependent upon defining the physiologic significance of coronary arterial stenoses demonstrated on coronary arteriograms. Accordingly, physiologic--angiographic correlates were studied in 12 anesthetized dogs prepared with an electromagnetic flowmeter and micrometer-controlled occluder on the circumflex coronary artery, a pair of sonic crystals in the myocardium within the distribution of the circumflex artery, and a catheter in the thoracic aorta. Measurement of arterial diameters on coronary arteriograms was made to define the minimum percent stenosis that caused: (1) decrease in resting coronary blood flow (CBFr); decline in the peak level of coronary blood flow (CBF) produced by intense vasodilatation induced by intracoronary infusion of ATP (CBFATP); and (3) segmental left ventricular (LV) dysfunction. CBFR decreased at an average stenosis of 80.45 +/- 9.13% (SD) (percent reduction in luminal diameter), while CBFATP declined at a stenosis of 31.83 +/- 5.64%. Segmental LV dysfunction was observed at a stenosis of 85.92 +/- 9.83%. In all dogs, the initial stenosis causing decline in CBFATP was a less than or equal to 40% reduction in luminal diameter. The results of this study indicate that coronary arterial stenoses of 40% or less may be hemodynamically significant under situations of augmented CBF. On the other hand, regional contractile function at rest is preserved up to stenosis in excess of 80%.

Effects of low osmolality contrast materials on coronary hemodynamics, myocardial function, and coronary sinus osmolality in normal and ischemic states.

The effects of intracoronary administration of contrast materials on regional and global left ventricular (LV) function and coronary sinus osmolality were assessed in six anesthetized dogs with segmental myocardial ischemia produced by critical stenosis of the circumflex coronary artery. Effects caused by Renografin (sodium meglumine diatrizoate), two new low osmolality contrast agents (Hexabrix and Hexabrix with added calcium ions), and metrizamide were evaluated. In a nonischemic state, Renografin produced an early (0-10 seconds) decrease in LV contractility followed by a late (10-20 seconds) rebound augmentation in contractility. In the presence of regional ischemia, there are prolongation of the depression of the myocardial contractile state. The monoacid dimer, Hexabrix, demonstrated a similar biphasic response, although the initial depression of myocardial contractility was significantly less than that observed with Renografin. Hexabrix with added calcium ions and metrizamide produced only augmentation in global and regional parameters of LV contractile function. This lack of depressant effects was also observed in the ischemic state. Renografin caused a significantly greater increase in coronary sinus osmolality (Tp) as compared with Hexabrix, Hexabrix-Ca++, and metrizamide. The increases in osmolality in response to the latter three contrast agents were statistically indistinguishable.

Cardiovascular effects of protamine sulfate.

Rapid administration of protamine sulfate after arteriography or cardiopulmonary bypass has occasionally been associated with marked hypotension. Since it is unclear whether this is due entirely to vasodilatation or to myocardial depression in addition to vasodilatation, the authors assessed the direct myocardial and systemic circulatory effects of this drug in seven anesthetized dogs. Direct effects of protamine sulfate on global and regional myocardial function and peripheral arterial resistance were determined in the presence and absence of segmental myocardial ischemia. Effects on the myocardium were determined by intracoronary administration of protamine; effects on the systemic circulation were determined after intravenous administration. Intracoronary administration of protamine caused no significant change in left ventricular contractility in either the normal or ischemic state. Intravenous administration produced hypotension due to peripheral vasodilation.