Effect of maximal coronary vasodilation on transmural myocardial perfusion during tachycardia in the awake dog.

Abstract

We studied the influence of active coronary vasomotion on transmural myocardial perfusion during tachycardia. Regional myocardial blood flow was estimated in chronically prepared awake dogs by injecting radioactive microspheres (7-10 /xm in diameter) into the left atrium. Studies were performed during ventricular pacing at 100, 150, 200, and 250 beats/min under control conditions with intact coronary vasomotor tone, and during maximal coronary vasodilation induced by intravenous infusion of adenosine. During control conditions, mean myocardial blood flow was 1.27 ± 0.12 ml/min per g of myocardium at a heart rate of 100 beats/min, and increased regularly with increasing heart rates. Transmural myocardial perfusion remained essentially uniform as heart rates were increased from 100 to 250 beats/min. During administration of adenosine, mean myocardial blood flow increased to 5.49 ± 0.39 ml/min per g at a heart rate of 100 beats/min, and transmural myocardial perfusion was uniform. As heart rates were increased, flow to the subendocardium decreased as a linear function of heart rate while subepicardial flow was maintained so that the ratio of subendocardial-subepicardial flow fell from 1.00 at a heart rate of 100 beats/min to 0.40 at a heart rate of 250 beats/min. The reduction of subendocardial perfusion with increasing heart rate was most marked in the deepest myocardial layers. This rate-dependent decrease in subendocardial blood flow resulted in a decrease in mean myocardial blood flow with increasing heart rates (mean change at 250 beats/min = -18%; P < 0.05). These data indicate that active coronary vasomotion is necessary for maintenance of uniform transmural myocardial perfusion during tachycardia.

Synergistic Adaptations to Exercise in the Systemic and Coronary Circulations That Underlie the Warm-Up Angina Phenomenon

“…4,6 It is well established that the subendocardial tissue layer is sensitive to the systolic flow impediment of cardiac contraction, especially in the presence of reduced coronary pressure resulting from a proximal stenosis, 27 and that the resultant hypoperfusion spreads from endocardium to epicardium. 4,7 Subendocardial flow therefore depends critically on diastolic duration.…”

“…4,7 Subendocardial flow therefore depends critically on diastolic duration. 5,6 At increased hearts rates, as the interval of diastole is reduced, active coronary vasodilatation is required to maintain transmural diastolic perfusion. 4,5 Exercise produces an intense vasodilatory stimulus on the coronary resistance vessels, which substantially alters the relative Figure 3.…”

“…4,5 With the onset of effort angina, the adaptation of the microvasculature is exhausted and resistance is thought to be near minimal, beyond the culprit coronary stenosis. 6,7 It is therefore surprising that symptoms and signs of myocardial ischemia can improve on second effort. Thus, the phenomenon of warm-up angina was an enigma that attracted the attention of early pioneers of physiological investigation in the cardiac catheterization laboratory.…”

Quantitative relationship between coronary vasodilator reserve assessed by 82Rb PET imaging and coronary artery stenosis severity

“…Multiple factors influence the shape and associated scatter of this relationship, including left ventricular haemodynamics, myocardial contractility, age-related changes in myocardial blood flow, collateral flow not visible on conventional angiography, and possibly others (20)(21)(22)(23)(24)(25). There are also inherent discrepancies between anatomical descriptors and functional behaviour of the human circulation.…”

Cardiac Troponin I Levels in Children with Acute Severe Asthma Treated with IV Salbutamol

“…One potential explanation to account for this association could lie in the relationship between heart rate and coronary perfusion during diastole. Since baseline and maximal heart rates vary inversely with age, it seems reasonable to speculate that cardiac myocytes of young children tolerate periods of sustained tachycardia, as might occur with salbutamol therapy, better than cardiac myocytes of older children [5].…”