Coronary Vascular Reserve Research Articles

Maximal coronary flow and the concept of coronary vascular reserve.

Maximal coronary flow and the concept of coronary vascular reserve.

Variable effects of intracoronary nitroglycerin on myocardial blood flow and segmental shortening according to dose and degree of coronary occlusion

The effects of intracoronary nitroglycerin were determined in 21 open-chest dogs. Six dogs with severe stenosis (25 mm Hg diastolic perfusion pressure) and nine dogs with moderate stenosis (40 mm Hg) received a 12 μg bolus followed by 44 μg/min intracoronary nitroglycerin. In addition, six dogs with moderate stenosis (40 mm Hg) received 5 μg followed by 5 μg/min nitroglycerin. Myocardial blood flow was measured with radioactive microspheres and segment shortening with ultrasonic crystals. At 40 mm Hg, high-dose but not low-dose nitroglycerin raised epicardial blood flow, while at 25 mm Hg nitroglycerin had no effect. Subendocardial blood flow was not affected in any group. Partial occlusion resulted in a decrease in segment shortening in the 25 mm Hg group but not at 40 mm Hg. High-dose nitroglycerin had no effect on shortening at either level of occlusion. Thus, in the presence of coronary vascular reserve, high-dose nitroglycerin may overcome coronary autoregulation. A dose equivalent to one that simulates the amount of nitroglycerin delivered to the coronary circulation by a systemic infusion did not affect myocardial blood flow. In addition, even a large dose of nitroglycerin did not affect segment shortening.

Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p <0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups. Infarctions that did not produce dyskinesia were very small (≤4% LV mass at 20 minutes and ≤6% LV mass at 2 days). In all but 3 dogs, dyskinesia at 20 minutes persisted at 2 days. In no dog did dyskinesia develop at 2 days if it was absent at 20 minutes. Thus, 2-D echo-demonstrated wall thickening abnormalities may be useful in the quantitative assessment of infarct size and coronary risk area.

Cardiovascular Effects of Pancuronium and Vecuronium during High-Dose Fentanyl Anesthesia

To define the role of muscle relaxants in hemodynamic responses to high-dose (75 μg/kg) fentanyl anesthesia, we compared the circulatory effects of pancuronium (Pc) with those of vecuronium (Vc) in patients about to undergo coronary artery bypass surgery. The first measurements were made while the patients were awake. Thereafter the patients were anesthetized with fentanyl, intubated under succinylcholine relaxation and mechanically ventilated with a mixture of oxygen in air (Flo2 0.50). Ten minutes after completion of the fentanyl injection, the second set of measurements was made. Immediately thereafter, 0.1 mg/kg of either Pc (n = 10) or Vc (n = 10) was given, and no relaxant was administered to 10 control patients. Heart rate (HR) and cardiac index (CI), which had decreased significantly after fentanyl induction, decreased further after Vc, the latter decreases being significantly greater than the decreases in HR and CI observed in control patients. After Pc, HR and CI increased to control a wake levels; rate-pressure product also increased and stroke index decreased. Five of ten patients receiving Vc had a HR below 45 beats/min; HRs this low were not seen in patients given Pc. Neither Pc nor Vc affected systemic vascular resistance, but filling pressures of the heart decreased abruptly after both relax-ants. We conclude that if maintenance of preanesthetic hemodynamic status is the objective of anesthetic management of patients having coronary artery bypass surgery, Pc helps to achieve this objective during high-dose fentanyl anesthesia. On the other hand, many patients with limited coronary vascular reserve may well benefit from the negative chronotropic effect of Vc.

Impaired coronary flow and ventricular function in hearts of hypertensive rats.

Hearts of rats made hypertensive (BP greater than 150 mmHg) by left renal artery clipping and sham operated controls were studied in two series of experiments. In series I, cardiac function was studied in an isolated working heart apparatus at weeks 4, 9 to 10 and 16 to 17 post-surgery. In series II, coronary flow was studied during normoxic and anoxic retrograde perfusions at days 6 to 9 and at weeks 4 and 10 post-surgery. In series I, when compared with controls, hypertensives had lower body weights at weeks 4 and 9 to 10, and higher left ventricular weights at each period. Heart function was depressed for hypertensives when compared with controls as measured by lower stroke volume, peak left ventricular systolic pressure, stroke work, ejection fraction, positive dP/dt, peak aortic flow, and maximal flow acceleration. Relaxation rate as measured by negative dP/dt was also depressed. Hearts from hypertensives had significantly lower coronary flows and MVO2, and increased percent oxygen extraction and effluent lactate/pyruvate ratios. LVEDP was significantly elevated for hypertensives, when LVEDV (ml) was similar for hypertensives and controls. Myocardial actomyosin ATPase activity was depressed for hypertensives at weeks 9 to 10 and 16 to 17 post-surgery. In series II, when hearts were perfused retrogradely, coronary flow was lower for hypertensives than for controls during normoxia at days 6 to 9 and at week 4, and during anoxia at all time periods. The findings demonstrate that impaired coronary vascular reserve develops within days of the development of hypertension in rats, and this can be associated with impaired ventricular function.

Regional myocardial blood flow and coronary vascular reserve in unanesthetized ponies during pacing-induced ventricular tachycardia

To examine the effects of tachycardia on coronary circulation, transmural distribution of myocardial blood flow (MBF, 15-μm diameter radionuclide-labeled microspheres) was studied in six healthy adult ponies at rest (heart rate = 60 ± 7 beats · min −1), during ventricular pacing at 150 and 200 beats · min −1, as well as with ventricular pacing at 250 beats · min −1 before and during maximal coronary vasodilatation (iv adenosine infusion; 4 μmole · kg −1 · min −1). Mean aortic pressure and cardiac output were unchanged from control values with ventricular pacing. Whereas ventricular pacing at 150 and 200 beats · min −1 resulted in a progressive uniform increase in transmural MBF and well-maintained endo:epi perfusion ratio, pacing at 250 beats · min −1 did not result in a further increase in MBF compared to pacing at 200 beats · min −1 and the left ventricular (LV) subendocardial:subepicardial (endo:epi) perfusion ratio was significantly less than 1.00 (0.87 ± 0.05). Blood flow to the LV papillary muscles and subendocardium was significantly less than that recorded at 200 beats · min −1. The LV endo:epi perfusion ratio with ventricular pacing at 250 beats · min −1 during adenosine infusion resulted in a decrease in mean aortic pressure (63% of control value) and a marked further reduction in blood flow to the LV papillary muscles as well as the LV subendocardium, while MBF increased dramatically in the LV subepicardium compared to values observed during ventricular pacing at 250 beats · min −1 alone. This resulted in a LV endo:epi perfusion ratio of 0.39 ± 0.09. By contrast, transmural right ventricular (RV) MBF increased significantly and the RV endo:epi perfusion ratio was well maintained. These data demonstrate that coronary vasomotion functions to maintain LV subendocardial blood flow in the pony myocardium at a heart rate of 200 beats · min −1, while at 250 beats · min −1 exhaustion of coronary vasodilator reserve in the deeper layers limits further increase in MBF.

Dynamic vascular factors in the genesis of myocardial ischemia

While fixed atherosclerotic and thrombotic lesions have long been known to cause myocardial ischemia and cardiac pain, the various transient or dynamic events that may also cause ischemia and pain have become better understood in the past 15 years. These can be classified into two broad categories: those that cause a dynamic reduction in the caliber of the coronary arteries and those that reduce the coronary vasodilatory reserve capacity. In the first group are myocardial compression or "bridging" of an artery; coronary vasoconstriction due to frank spasm or generalized arterial hypertonus, particularly at the site of atherosclerotic lesions; reduced arterial distending pressure and platelet aggregation which may transiently occlude a diseased arterial segment. The causes of inadequate coronary vascular reserve flow capacity can be either anatomic or functional. Among the former, the increased muscle mass to blood vessel ratio occurring in myocardial hypertrophy is most important. The functional causes of limited coronary vascular reserve include diastolic transmural compression and coronary "steal," both of hemodynamic origin. In addition, arteriolar "unresponsiveness" or dysregulation caused by smoking, drugs or other unknown conditions may adversely affect coronary vascular reserve. Hence, myocardial ischemia may result from conditions that limit potential for increase in flow or from conditions that reduce flow from a preexisting level. These conditions, which are transient and dynamic in nature, may modify the threshold for ischemia, particularly in patients with fixed coronary obstructive disease.

Effects of chronic tobacco smoking on the coronary circulation

The effects of chronic smoking on the coronary circulation were studied by evaluating the coronary vascular reserve in 12 chronic smokers (group 1) and 10 nonsmokers (group 2). All patients were referred to cardiac catheterization for evaluation of chest pain and were found to have normal coronary and left ventricular angiograms. Coronary vascular reserve was measured by analyzing the hyperemic response to selective coronary injection of contrast agent. There was no statistically significant difference between groups 1 and 2 with regard to age, baseline electrocardiogram or response to treadmill or thallium-201 exercise tests. The mean coronary reserve (+/- standard deviation) was 74.1 +/- 20.1% in the smokers versus 117.1 +/- 45.1% in the nonsmokers (p less than 0.02). In patients who smoked 1 pack a day or less and in those who smoked more than 1 pack a day, the mean coronary reserve was 89.5 and 64.9%, respectively (p less than 0.05). Additionally, of 20 patients followed up for an average of 20 months, 7 of 10 smokers and 1 of 10 nonsmokers continued to have chest pain (p less than 0.03). The cause for the chest pain has not been established in these patients. These results suggest that coronary vascular reserve is significantly less in chronic smokers than in nonsmokers, and that this decrease is more pronounced in heavy smokers.

Coronary vascular reserve in left ventricular hypertrophy secondary to chronic aortic regurgitation

Coronary vascular reserve was studied in 11 patients with severe chronic aortic regurgitation (AR). Nineteen patients with the chest pain syndrome and normal findings on cardiac catheterization served as control subjects. Resting coronary sinus flow and contrast-agent-induced hyperemia were measured by continuous thermodilution. Left ventricular (LV) dimensions and mass were obtained echocardiographically. All patients had normal coronary arteries. Resting coronary flow was increased and coronary reserve was decreased in patients with AR compared with the control subjects: 310 +/- 38 versus 121 +/- 13 ml/min and 56 +/- 9 versus 86 +/- 7.5%, respectively. The decrease in coronary vascular reserve correlated with the increase in LV mass (r = -0.86, p = 0.001) and LV wall thickness (r = -0.83, p = 0.002) and with the decrease in LV volume/mass ratio (r = 0.761, p = 0.007). There was no significant correlation between the decrease in coronary vascular reserve and LV volume (r = 0.255), LV peak wall stress (r = 0.292), LV systolic pressure (r = -0.495), aortic or LV diastolic pressure (r = 0.322 and -0.318, respectively), or aortic-LV diastolic gradient, nor with the voltage on the electrocardiogram (limb leads r = -0.60, precordial leads r = -0.118). Thus, coronary vascular reserve is decreased in proportion to the degree of left ventricular hypertrophy in patients with chronic AR. Patients with angina pectoris tended to have a lower coronary vascular reserve than those without angina (median 26 versus 76%, difference not significant). LV wall thickness and not LV volume is the critical component of left ventricular mass related to coronary reserve. No significant correlation between the decrease in coronary vascular reserve and the presence of angina pectoris was demonstrated.

Measurements of coronary blood flow and degree of stenosis: Current clinical implications and continuing uncertainties

Initial measurements of coronary blood flow in human beings were limited by methodologic inadequacies causing clinically important areas of reduced perfusion to be incompletely represented or overlooked. More recent measurements have provided insight into clinically relevant pathophysiology. There has been increasing appreciation of the need for values of flow to be related to concomitant myocardial oxygen demand, and of the importance of evaluating perfusion in relation to coronary vascular reserve. Regional flow measurement techniques have progressed significantly during the past decade and have provided better insight into perfusion deficits in ischemic heart disease. A greatly improved understanding of the relation between the arteriographic degree of stenosis and perfusion limitation also has developed, in reviewing studies addressing these points, the present article attempts to highlight their current clinical implications and address continuing uncertainties meriting further attention.

Coronary hemodynamic effects of angiotensin inhibition by captopril and teprotide in patients with congestive heart failure

The coronary hemodynamic effects of vasodilator therapy with angiotensin-converting enzyme inhibitors (captopril arid teprotide) were studied in 11 patients with ischemic heart disease and severe congestive heart failure (CHF). Over 2 hours, systemic vascular resistance was reduced from 2,408 ± 240 to 1,715 ± 170 dynes·s·cm −5 (p < 0.001), and cardiac output improved 18%, resulting in lower arterial pressure (101 ± 8 to 86 ± 5 mm Hg, p < 0.001) and left ventricular filling pressure (30 ± 2 to 21 ± 2 mm Hg, p < 0.001). Coronary sinus thermodilution blood flow parallelled perfusion pressure but did not significantly vary overall (160 ± 20 to 133 ± 12 ml/min, difference not significant [NS]). Coronary vascular resistance was unchanged. Although the left ventricular stroke work index rose slightly (37.7 ± 8.8 to 41.3 ± 7.9 g·m/m 2, p < 0.05), there was no change in the coronary arteriovenous oxygen content difference (10.8 ± 1.0 to 10.4 ± 1.0 ml/100 ml, NS) or calculated myocardial oxygen consumption (16.4 ±1.9 to 13.9 ± 1.6 ml/min, NS). The heart rate-systolic blood pressure product declined significantly during this period (8,824 ± 703 to 7,087 ± 514 beats·mm Hg, p < 0.02); this relief of cardiac effort was a function of the pretreatment plasma renin activity. A derived index of external myocardial efficiency improved 37% (19 ± 3 to 26 ± 6, p < 0.05), reflecting greater left ventricular work without increased oxygen demand. Enhancement of myocardial performance after converting enzyme inhibition appears dependent on reduction of angiotensin-mediated ventricular afterload and preload. The lack of coronary vasomotor effects in patients with advanced ischemic cardiomyopathy may reflect limited coronary vascular reserve. Improvement of heart failure in these patients developed without evidence of myocardial ischemia, since balance was maintained between oxygen supply and demand.

Effects of physical training on myocardial vascularity and perfusion.

Physical training is thought to be a stimulus for coronary vascular growth and coronary collateral development. This report is a summary of knowledge in the area. Studies in experimental animals with normal hearts indicate that physical training promotes increased myocardial capillary density and also causes enlargement of the surface coronary vessels. The physiologic effect of these changes on coronary vascular reserve and protection of segments of the heart against myocardial ischemia has not been established. Physically trained dogs and pigs do not appear to be protected against the effects of coronary occlusion, in that the ischemic area appears to be as large in trained animals as in untrained animals for any given coronary lesion. One study in physically trained rats appears to show protection against myocardial infarction, but whether this is related to coronary vascular changes has not been established. Experiments in dogs subjected to chronic narrowing or gradual occlusion demonstrate that physical training in these models does promote collateral blood flow as measured by retrograde flow in open-chest experiments. Studies using the microsphere technique in closed-chest animals confirms increased collateral flow to ischemic areas in some animals, but the magnitude of the increases appears to be small and varies greatly from animal to animal. Studies in athletes suggest that myocardial blood flow is lower at any submaximal level of training in athletes than in sedentary persons. Studies in patients with coronary artery disease have generally failed to show an increase in coronary blood flow or in perfusion of ischemic areas after physical training programs, but the techniques used might not have been sensitive enough to detect changes. The evidence in the experimental animals is sufficiently promising to indicate that the search should be continued to define physical training programs that will most stimulate myocardial vascularity and coronary collaterals in humans.

Regional myocardial blood flow and coronary vascular reserve in unanesthetized young calves exposed to a simulated altitude of 3500 m for 8--10 weeks.

We determined regional myocardial blood flow (15-micrometer tracer microspheres) and hemodynamics in nine normal calves, seven calves with right ventricular (RV) hypertrophy induced by pulmonary artery banding (PAB) at sea level, and five calves exposed to simulated high altitude (HA) of 3,500 m (PB = 500 mm Hg) for 8--10 weeks. Progression of RV hypertrophy was very rapid in HA calves. RV weight:body weight ratio of 2.74 +/- 0.20 g/kg at 8--10 weeks of sojourn at HA significantly exceeded that in PAB calves (1.98 +/- 0.11 g/kg) 20 weeks post-banding. All calves were studied unanesthetized at sea level before (control) and during maximal coronary vasodilation (iv adenosine; 4 microM/kg per min). Normal and HA calves were also studied during acute hypoxemia (PaO2: 42 +/- 1 mm Hg) induced by administration of 12--13% O2 + N2 in the inhaled gas. RV myocardial blood flow was significantly increased only in PAB calves, whereas in HA calves it was similar to that in normal calves. Left ventricular (LV) mass and blood flow were identical in three groups of calves. Polycythemia did not occur in HA calves. Minimal coronary vascular resistance per unit weight of the hypertrophied RV was identical to that in the normal RV myocardium. This suggested that, despite very fast progression of RV hypertrophy in HA calves, functional cross-sectional area of the RV coronary vascular bed kept pace with the increase in cardiac mass. Minimal coronary vascular resistance per unit weight of the left ventricular myocardium was also identical in three groups of calves. This suggested that chronic hypoxemia by itself did not cause an increase in the functional cross-sectional area of the LV coronary vascular bed. Acute hypoxemia resulted in a significant increase in myocardial blood flow in all calves, but in HA calves, RV endo:epi perfusion ratio decreased below 1.00. Transmural RV myocardial blood flow and RV systolic pressure in HA calves during acute hypoxemia significantly exceeded that in normal calves.

Greater Coronary Vascular Reserve in Dogs Anesthetized with Halothane

Greater Coronary Vascular Reserve in Dogs Anesthetized with Halothane

Coronary hemodynamics in simulated paroxysms of ventricular tachycardia: role of myocardial impairment and of extravascular resistance.

In 6 patients with healthy hearts (controls), 17 with coronary artery disease (CAD) and 6 with left ventricular hypertrophy due to aortic valvular disease, aortic pressure, coronary sinus blood flow (CSF) and lactate extraction were determined before and after the sudden onset of a paced ventricular tachycardia of 170 bpm (VT 170 = simulated paroxysmal ventricular tachycardia). Comparison to parameter changes during dipyridamol vasodilation revealed reduced coronary vascular reserve for CAD and hypertrophy. While VT induced a reduction of aortic pressure (stabilized by an average of 22%, and most excessively for CAD; p less than 0.05) and CSF remained at/or slightly above control levels (by an average of 31%; p greater than 0.05) equally for all groups (p greater than 0.05), lactate production in the groups with CAD and hypertrophy indicated myocardial impairment by ischemia. Excessively greater increases of CSF during dipyridamol vasodilation (vs. VT) for all groups suggested VTs extravascular resistance increase to have limited the extent of the potential of coronary vascular decrease. With one variable being kept constant (i.e. 'clamping' the vascular component of coronary resistance at its limit by dipyridamol), tachycardia during dipyridamol (D) vasodilation (VT 170+D and VT 140+D) in the controls and in the CAD group resulted in a linear decrease of CSF, allowing quantification of impaired coronary reserve for CAD. We concluded from the observations that: (1) paroxysmal VT demands fast therapeutic action foremost in the impaired myocardium, and (2) tachycardia per se acts as limiting factor for coronary blood flow via increase in extravascular resistance (aside from a shortened diastole).

Disturbances in coronary microcirculation (author's transl)

The clinical syndrome "coronary insufficiency at normal coronary arteriogram" is found in approximately 10-20 per cent of patients with exercise-induced coronary insufficiency. In most of these cases disturbances of coronary microcirculation are present. They can appear in vascular diseases (arterial hypertension, systemic immunopathies, immune complex vasculitis etc.), in rheological diseases (paraproteinemia, hyperlipoproteinemia, polyglobulia etc.) and in disturbances of transport and diffusion of oxygen (carbon monoxide intoxication, methemoglobinemia, hyperlipoproteinemia). The clinical diagnosis is based on usual diagnostic programs (electrocardiogram, exercise electrocardiogram, responsiveness to nitroglycerin etc.), as well as on a newer, functionally orientated diagnostic procedures (determinations of coronary blood flow and of coronary vascular reserve, production of lactate, serological findings, histology and immune histology of peripheral arteries, measurements of viscosities in both, plasma and blood etc.). Many clinically relevant disturbances in coronary microcirculation can thus be detected and therefore can be treated on a rational basis by the management of the internal main disease, this is by the treatment of the vascular, rheological and metabolic disorders. Persistent angina pectoris, in the presence of normal coronary arteriogram, represents no termination of coronary diagnostics, but moreover implies the clinical task for using newer diagnostic possibilities in order to enable functional and therapeutical assessment of coronary microcirculation.

Blood flow in the hypertrophied right ventricular myocardium of unanesthetized ponies.

To examine the effects of right ventricular (RV) hypertrophy on regional myocardial blood flow and coronary vascular reserve, hemodynamics and myocardial blood flow (15-micrometers radio-nuclide-labeled microspheres) were studied in 12 unanesthetized adult ponies before and during intravenous isoproterenol HCl infusion (1 microgram.kg-1.min-1). Six ponies served as controls, whereas in each of the others the main pulmonary artery (PA) had been banded 35-90 days prior to the study. Marked RV hypertrophy was present in PA-banded animals. In these ponies, there was a significant increase in RV systolic pressure (147%), heart rate (88%), RV tension-time index (279%), and RV myocardial blood flow (137%), while their RV coronary vascular resistance was only 40% of that for control ponies. Blood flow in right side of the interventricular septum was also significantly higher in the PA-banded ponies. Endo/epi perfusion ratio exceeded 1.00 for both ventricular freewalls in all animals. With isoproterenol infusion, there was a marked increase in myocardial blood flow in both groups. However, in PA-banded ponies the endo/epi flow ratio decreased precipitously below 1.00 in both ventricular freewalls. In control ponies this did not happen in the RV freewall, and RV coronary vascular resistance decreased to 19% of its control value. In PA-banded ponies, the magnitude of decline in RV coronary vascular resistance was much smaller, only 32% of that for control ponies. It is concluded that, unlike in LV hypertrophy, transmural myocardial blood flow per unit mass is much higher in the hypertrophied RV myocardium of adult resting ponies, and this higher RV perfusion occurs at the expense of curtailed RV coronary vascular reserve.

Coronary flow studies in patients with left ventricular hypertrophy of the hypertensive type: Evidence for an impaired coronary vascular reserve

Increased myocardial blood flow occurs in ventricular hypertrophy, but flow per 100 grams of myocardium remains normal. The increase in flow may be obtained at the expense of the existing coronary vascular reserve or by an increase in the vascular bed. The coronary vascular reserve was studied by analyzing the hyperemic reaction to selective injection of contrast agent into the coronary arteries in 25 patients: a control group (9 patients) with chest pain syndrome, normal coronary arteries and a normal left ventricle (Group I) and 16 patients with aortic stenosis, left ventricular hypertrophy and normal coronary arteries (Group II). The hyperemic response in Groups I and II was 73.3 ± 2.2 and 65.8 ± 9.1 percent, respectively (difference not significant). Group II was subdivided into two groups: Group IIA had five patients with a left ventricular mass of less than 200 g (mean 158.8 ± 25.9); this group had a hyperemic response of 102.3 ± 9.9 percent. Group IIB had 11 patients with a left ventricular mass of more than 200 g (mean 308.9 ± 22.5) and a hyperemic response of 49.27 ± 10.42 percent. The hyperemic response was correlated with the diastolic left ventricular-aortic gradient (r = +0.64, p < 0.001), left ventricular mass (r = −0.51, p < 0.01) and aortic diastolic pressure (r = +0.636, p < 0.001). Group I had a left ventricular mass similar to that of Group IIA (124.9 ± 9 and 158.8 ± 26 g, respectively) but a lower hyperemic response (73.3 ± 2 and 102.3 ± 10 percent, respectively). These data suggest that severe left ventricular hypertrophy is associated with a reduction in coronary vascular reserve; it is speculated that this decrease in the vascular reserve capacity may be related to the ischemie component of hypertrophic heart disease.

Regional coronary blood flow and coronary vascular reserve in unanesthetized calves at rest and during pharmacologic stress

The present study was carried out: (a) To determine whether the uniformity of transmural left ventricular (LV) myocardial blood flow (MBF) is due to a gradient of vasoactive tone or to a gradient of vascularity favoring the deeper layers. (b) To examine the changes in right ventricular (RV) MBF and coronary vascular reserve of conscious calves brought about by various kinds of stress. Hemodynamics and MBF (15-μm tracer microspheres) were studied in six awake calves before and during maximal coronary vasodilatation induced by adenosine infusion (4 μ M/kg/min). Although heart rate increased by 46% and mean aortic blood pressure decreased by 29% with adenosine infusion, the RV and LV MBF had increased by 710 and 394%, respectively. Thus under basal conditions we found RV coronary vascular reserve to be greater than that in the LV. The endo:epi ratio during maximal coronary vasodilatation did not decrease below 1.00 in both ventricles. This suggested that normally higher LV subendocardial perfusion (i.e., endo:epi > 1.0) of resting awake calves is most likely not due to a out → in diminishing gradient of vasomotor tone. Minimal coronary vascular resistance was identical for both ventricles. MBF was also studied in six additional calves at control, during isoproterenol infusion (0.2 μg/kg/min), pacing, and acute volume overload before and after propranolol pretreatment. The percentage increase in RV MBF per unit weight was higher than that in the LV MBF with each stress. With isoproterenol stress, LV endo:epi had decreased significantly below 1.0 while RV endo:epi was well maintained. Propranolol pretreatment significantly blunted the increase in RV and LV MBF brought about by acute volume overload.

The pathophysiology of failure in acute right ventricular hypertension: hemodynamic and biochemical correlations.

Acute right ventricular (RV) hypertension and failure occur clinically. In this study we examined the mechanism of RV failure. Adult dogs were studied acutely under anesthesia; dogs were instrumented for measurement of pressures and right coronary artery blood flow. Myocardial blood flow and cardiac output were determined with radionuclide-labeled microspheres, and the presence of ischemia was determined by biochemical analysis of ventricular biopsies. RV hypertension was produced by constricting the pulmonary artery and was increased until RV failure occurred, as evidenced by decreased aortic pressure and cardiac output and increased RV end-diastolic pressure. With increasing RV systolic pressure, RV myocardial blood flow failed to increase in proportion to demand. At the onset of RV failure, there was no reactive hyperemia of right coronary flow compared with control, indicating the absence of further coronary vascular reserve; biochemical analysis demonstrated that the RV free wall was ischemic; the LV free wall was not. Infusion of phenylephrine raised aortic pressure and hence, myocardial perfusion pressure; RV failure reversed as shown by decreased RV end-diastolic pressure and increased cardiac output and RV systolic pressure; reactive hyperemia of right coronary flow was restored and the biochemical indexes of ischemia were reversed, demonstrating that ischemia is the cause of failure in acute RV hypertension.