Left Ventricular Myocardial Blood Flow Research Articles

Measurement of left ventricular heat production in man

A system to measure left ventricular heat production phi iv in conscious human subjects is described. Using phi iv and the rate of energy supply to the myocardium, the mechanical efficiency of the left ventricle is calculated. Heat carriage in left ventricular myocardial blood flow phi cs is calculated from coronary sinus flow and the transcoronary temperature difference. Diffusional heat loss phi diff is derived from the ratio of areas under temperature/time curves recorded in the aorta and coronary sinus after a bolus injection of cold saline into the pulmonary artery. The sum of phi cs, phi diff and phi chem (the energy of endothermic reactions with haemoglobin) gives phi iv. The estimated errors in the derived values of heat production and mechanical efficiency are less than 17 per cent. At basal heart rates 17 patients with good left ventricular function had a transcoronary temperature difference of 0.16 +/- 0.03 degrees C (mean +/- standard deviation), left ventricular flow blood of 145.3 +/- 81.5 ml min-1, and phi iv of 3.1 +/- 1.8 W. Left ventricular oxygen extraction was strongly correlated with phi iv (r = 0.925, p less than 0.001). Left ventricular mechanical efficiency was 0.33 +/- 0.11, at basal heart rates, which fell to 0.18 +/- 0.15 (p less than 0.001) on atrial pacing at 100 beats min-1.

Coronary vascular smooth muscle function in E. coli endotoxemia in dogs

The purpose of this study was to determine whether intrinsic contraction-relaxation properties of coronary arteries are altered during acute gram-negative endotoxemia. Coronary vascular smooth muscle (VSM) was evaluated in vitro using large and small left circumflex coronary ring preparations isolated from dogs 4 h after administration of either saline (control; C) or 1.5 mg/kg Escherichia coli endotoxin (ET). ET dogs exhibited marked systemic hypotension and cardiovascular depression throughout the 4-h in vivo phase of the study accompanied by reduction in total left ventricular myocardial blood flow. Isolated coronary vessels were stretched to the apex of the length-contractile tension curve; no differences were observed in length-active or length-passive tension (vessel compliance) relationships between C and ET vessels. Isometric contractions produced by K+ and prostaglandin F2 alpha (PGF2 alpha) were similar in C and ET coronary arteries. VSM relaxant responses to nitroprusside (NP; 10(-10) to 10(-4) M) were also similar in C and ET vessels. In contrast to the apparent lack of effect of ET on directly acting VSM agents, relaxation responses to the endothelial-dependent vasodilator acetylcholine (ACh) were significantly less in ET vessels. Impaired vasodilator response to ACh was not improved by in vivo treatment with the combination antioxidant therapy of allopurinol, superoxide dismutase, and catalase. We conclude that both depolarization (K+) and receptor (PGF2 alpha)-mediated contractile mechanisms, as well as basal cGMP (NP)-mediated vasodilator mechanisms, remained functional in coronary vasculature during acute endotoxemia. Inhibition of ACh-mediated relaxation in ET vessels suggests altered endothelial-dependent vasodilation in coronary arteries during endotoxemia, but this change did not seem to be associated causally with oxygen free radicals.

Regional myocardial blood flow and left ventricular diastolic properties in pacing-induced ischemia

The relation between left ventricular diastolic abnormalities and myocardial blood flow during ischemia was studied in eight open chest dogs with critical stenoses of the proximal left anterior descending and circumflex coronary arteries. The heart was paced at 1.7 times the heart rate at rest for 3 min. In dogs with coronary stenoses, left ventricular end-diastolic pressure increased from 8 +/- 1 to 14 +/- 2 mm Hg during pacing tachycardia (p less than 0.01) and 16 +/- 3 mm Hg (p less than 0.01) after pacing, with increased end-diastolic and end-systolic segment lengths in the ischemic regions. Left ventricular diastolic pressure-segment length relations for ischemic regions shifted upward during and after pacing tachycardia in dogs with coronary stenoses, indicating decreased regional diastolic distensibility. In dogs without coronary stenoses, the left ventricular diastolic pressure-segment length relation was unaltered. Pacing tachycardia without coronary stenoses induced an increase in anterograde coronary blood flow (assessed by flow meter) in both the left anterior descending and circumflex coronary arteries, and a decrease in regional vascular resistance. In dogs with coronary stenoses, regional vascular resistance before pacing was decreased by 18%; myocardial blood flow (assessed by microspheres) was unchanged in both the left anterior descending and circumflex coronary artery territories. During pacing tachycardia with coronary stenoses, regional coronary vascular resistance did not decrease further; subendocardial myocardial blood flow distal to the left anterior descending coronary artery stenosis decreased (from 1.03 +/- 0.07 to 0.67 +/- 0.12 ml/min per g, p less than 0.01), as did subendocardial to subepicardial blood flow ratio (from 1.04 +/- 0.09 to 0.42 +/- 0.08, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of different doses of epinephrine on myocardial perfusion and resuscitation success during cardiopulmonary resuscitation in a pig model

Published results of dose-response effects of adrenergic drugs (epinephrine [E]) vary so much between studies because of differences in animal models and duration of ischemia before drug administration. In this investigation the effects of different doses of E on coronary perfusion pressure (CPP), left ventricular myocardial blood flow (MBF) and resuscitation success were compared during closed-chest cardiopulmonary rest scitation (CRP) after a 4-minute period of ventricular fibrillation in 28 pigs. MBF was measured during normal sinus rhythm using tracer microspheres. After 4 minutes of ventricular fibrillation CPR was performed with the use of a pneumatic piston compressor. After 4 minutes of mechanical measures only, the animals were randomly allocated into four groups of seven, receiving 0.015, 0.030, 0.045, and 0.090 mg/kg E intravenously respectively. MBF measurements were started 45 seconds after E administration; hemodynamic measurements after 90 seconds. Four minutes after the first administration, the same E dose was given before defibrillation. The CPP of animals given 0.015, 0.030, 0.045 and 0.090 mg/kg E were as follows: 16.3 ± 6.1, 25.6 ± 5.8, 33.2 ± 8.4 and 30.4 ± 6.3 mm Hg. The left ventricular MBF values were: 14 ± 9, 27 ± 11, 43 ± 6, 46 ± 10 mL/min/100 g. The differences between the groups receiving 0.015 and 0.045 mg/kg and between the groups receiving 0.015 mg/kg and 0.090 mg/kg were statistically significant ( P < .05). Resuscitation success was 14.3%, 42.9%, 100% and 86.7% respectively. A significant difference in resuscitation success was found only betwen 0.015 mg/kg and 0.045 mg/kg E. Our results suggest that after a 4-minute period of arrest and 4 minutes of CPR, CPP, MBF and resuscitation success are increased when E is given at a dosage of up to 0.045 mg/kg; however, the increase to 0.090 mg/kg does not lead to any further improvement.

移植心の心機能回復時間に関する実験的研究 単純浸漬保存心における保存時間別検討

移植心の心機能回復時間に関する実験的研究 単純浸漬保存心における保存時間別検討

Comparative effects of pacing-induced and flow-limited ischemia on left ventricular function.

We compared left ventricular (LV) myocardial blood flow and function accompanying severe demand ischemia (rapid atrial pacing in the presence of critical bilateral coronary stenoses) and supply ischemia (complete bilateral coronary occlusion) of the same ischemic regions in 14 pentobarbital-anesthetized dogs. Pacing-induced ischemia resulted in pronounced reductions in average regional epicardial blood flow (0.8 +/- 0.4 vs. control 1.2 +/- 0.4 [+/- SD] ml/g/min, p less than 0.05) and endocardial blood flow (0.4 +/- 0.1 vs. control 1.3 +/- 0.3 ml/g/min, p less than 0.05). More severe reductions in average regional epicardial and endocardial blood flow were seen after bilateral coronary occlusion (BCO) (0.3 +/- 0.3 and 0.1 +/- 0.1 vs. control 1.3 +/- 0.3 ml/g/min, p less than 0.05, respectively). Hemodynamics of postpacing ischemia (PPi) were consistently characterized by systolic impairment including depressed systolic contractile performance [(+)dP/dtmax 1,281 +/- 442 vs. control 2,173 +/- 775 mm Hg/sec, p less than 0.05], ventricular dilation (left ventricular [LV] end-diastolic dimension [EDD] 47.6 +/- 7.8 vs. control 44.7 +/- 8.6 mm, p less than 0.05), and an increase in LV end-diastolic pressure (EDP) (14.4 +/- 2.8 vs. control 4.2 +/- 2.8 mm Hg, p less than 0.05). Abnormalities in early and late diastolic function with PPi included increased time constant of isovolumic relaxation (78.0 +/- 40.4 vs. control 46.4 +/- 20.5 msec, p less than 0.05) and increased chamber stiffness (1.9 +/- 0.77 vs. control 0.81 +/- 0.55 mm Hg/mm, p less than 0.05), respectively. The LV diastolic pressure-dimension relation, however, shifted upward and to the right in eight of nine animals, whereas an upward shift was observed in only one animal. Thus, in this model of postpacing ischemia, we observed contractile failure and passive changes in diastolic function. Alterations in ventricular function occurred consistently earlier and to a greater extent during BCO than PPi, including higher LVEDP (25.3 +/- 8.1 vs. 14.9 +/- 6.6 mm Hg, p less than 0.05), greater ventricular dilation (delta LVEDD 4.9 +/- 2.5 vs. 3.5 +/- 2.8 mm, p less than 0.05), and reduced minor-axis dimension shortening (3.3 +/- 3.1% vs. 6.5 +/- 3.6%, p less than 0.05). To detect potential qualitative differences in ventricular function between the two types of ischemia, we evaluated hemodynamics at comparable loading conditions (30 seconds to 1 minute of BCO).(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of nitroprusside on myocardial blood flow and oxygen consumption in conscious lambs with an aortopulmonary left-to-right shunt.

We studied the effect of vasodilation on regional myocardial blood flow and oxygen consumption of the left ventricular free wall by infusing 10 micrograms/kg/min sodium nitroprusside into 7-week-old conscious lambs with and without aortopulmonary left-to-right shunts. Resting myocardial oxygen consumption in the 13 shunt lambs was significantly higher than in the nine control lambs (989 +/- 104 [+/- SEM] vs. 432 +/- 41 mumol/min/100 g left ventricle). This was achieved by a significantly higher left ventricular myocardial blood flow (294 +/- 33 vs. 143 +/- 16 ml/min/100 g left ventricle) because the arteriovenous oxygen concentration difference across the left ventricular free wall was similar in shunt and control lambs. Infusion of nitroprusside did not significantly change myocardial oxygen consumption and regional myocardial blood flows at 10 and 50 minutes after the onset of the infusion. This occurred despite a substantial drop in aortic and left atrial pressures and stroke volume, which decreases wall stress as well as external work of the left ventricle. Heart rate, however, increased significantly. We postulate that, during infusion of nitroprusside, the potential decrease in myocardial oxygen consumption due to a decrease in wall stress and external work of the left ventricle is neutralized by the consequences of the increased heart rate. In view of this and because of its hemodynamic effects, we do not consider sodium nitroprusside useful in the treatment of circulatory congestion in patients with left-to-right shunts, normal arterial pressures, and normal systemic blood flows.

Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs

Although large doses of epinephrine increase coronary perfusion pressure and flow during cardiopulmonary resuscitation, epinephrine also increases myocardial oxygen consumption during ventricular fibrillation. To test the hypothesis that epinephrine improves the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation, myocardial adenosine 5'-triphosphate (ATP) and lactate concentrations were measured before and immediately after 10 minutes of cardiopulmonary resuscitation in 10 control dogs and 10 dogs given intravenous epinephrine (1-mg bolus followed by 0.2 mg/min). Left ventricular myocardial blood flow during cardiopulmonary resuscitation was measured with radioactive microspheres and was significantly higher in the epinephrine group (48 +/- 11 vs. 21 +/- 4 ml/min/100 g, p less than 0.05). However, myocardial lactate concentration increased significantly (p less than 0.01) after cardiopulmonary resuscitation in both groups and tended to increase more in epinephrine-tre...

Beta-adrenergic influence on increased myocardial oxygen consumption during hypoxemia in awake newborn lambs.

The purpose of this investigation was to determine the role of increased beta-adrenergic activity in regulating the increase in myocardial oxygen consumption that occurs during hypoxemia in unanesthetized newborn lambs. Through a left thoracotomy, fluid-filled catheters were placed in the ascending aorta, coronary sinus and left atrium, a pressure transducer was introduced into the left ventricle, and pacing wires were sutured onto the left atrium. The lambs were studied 3 d later by making intermittent measurements of aortic and coronary sinus blood oxygen saturations and Hb concentrations, left ventricular myocardial blood flow, cardiac output, heart rate, left atrial and aortic blood pressures, the maximal first derivative of left ventricular pressure, aortic and coronary sinus blood oxygen contents, the arteriovenous difference of oxygen across the left ventricular myocardium, myocardial oxygen consumption, and external cardiac work (aortic mean blood pressure times cardiac output). In nine lambs with an intact beta-adrenergic nervous system (group 1), the above measurements were made during a control period and during hypoxemia (FiO2 = 0.08-0.10) with spontaneous tachycardia. In another group of 12 lambs (group 2), the measurements were made during a control period, after beta-blockade (1.5 mg/kg intravenous propranolol) with pacing at the control heart rate, during hypoxemia with pacing at the control heart rate, and during hypoxemia with pacing-induced tachycardia. In the group 2 lambs, beta-blockade completely inhibited the increase in heart rate, maximal first derivative of left ventricular pressure, cardiac output and cardiac work that occurred during hypoxemia in the group 1 lambs that had an intact beta-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of phospholipase A 2 inhibition on experimental infarct size, left ventricular hemodynamics and regional myocardial blood flow

It has been reported that activation of phospholipase A 2 and the subsequent degradation of membrane phospholipids are responsible for irreversible myocardial injury. Thus, we examined whether a phospholipase A 2 inhibitor 1-(benzylmethyl-amino)-3-[(α,α,α-trifluoro-m-tolyl)oxy]-2-propanol hydrochloride, can reduce myocardial necrosis after coronary artery occlusion. In 14 anesthetized dogs, 1 minute after coronary occlusion, 99mTc-labeled albumin microspheres (8 mCi) were injected into the left atrium for future assessment of the hypoperfused zone. After 15 minutes, the dogs were randomized to a control group ( n = 7) and a treated group ( n = 7, 2 mg/kg i.v.). After 6 hours, infarct size and hypoperfused zones were measured using triphenyltetrazolium chloride staining and autoradiography, respectively. The hypoperfused zone, as a percentage of the left ventricle, was 26 ± 3% and 23 ± 1% in the control and the treated groups (NS), respectively. The percentage of the hypoperfused zone that evolved to necrosis was 98 ± 4% in the control group and 45 ± 10% in the treated group ( P < 0.001) showing a reduction of 54%. By weight, in the control group, necrosis involved 26 ± 4 g of the left ventricle while in the treated group it was 9 ± 2 g ( P < 0.005). In 6 additional dogs, left ventricular hemodynamics and regional myocardial blood flow were studied before and after treatment i.e., 15 and 30 minutes after coronary occlusion, respectively. Phospholipase A 2 inhibitor did not acutely change heart rate, aortic pressure, left ventricular end-diastolic and systolic pressures, left ventricular dP dt and regional myocardial blood flow. Thus, phospholipase A 2 inhibitor salvaged the acutely ischemic myocardium, reducing necrosis by over 50% in the canine model. It is postulated that since this effect was not related to the studied hemodynamic parameters and regional myocardial blood flow, it may be related to the preservation of membrane integrity.

Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs.

Although large doses of epinephrine increase coronary perfusion pressure and flow during cardiopulmonary resuscitation, epinephrine also increases myocardial oxygen consumption during ventricular fibrillation. To test the hypothesis that epinephrine improves the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation, myocardial adenosine 5'-triphosphate (ATP) and lactate concentrations were measured before and immediately after 10 minutes of cardiopulmonary resuscitation in 10 control dogs and 10 dogs given intravenous epinephrine (1-mg bolus followed by 0.2 mg/min). Left ventricular myocardial blood flow during cardiopulmonary resuscitation was measured with radioactive microspheres and was significantly higher in the epinephrine group (48 +/- 11 vs. 21 +/- 4 ml/min/100 g, p less than 0.05). However, myocardial lactate concentration increased significantly (p less than 0.01) after cardiopulmonary resuscitation in both groups and tended to increase more in epinephrine-treated animals. Myocardial ATP concentration decreased significantly (p less than 0.05) and by comparable amounts in the two groups. These findings suggest that large doses of epinephrine may fail to improve the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation, even when they result in a substantial increase in coronary blood flow.

Metabolic protection of the reperfused canine endocardium by the thromboxane synthetase inhibitor, dazoxiben

This study investigated whether dazoxiben, a thromboxane synthesis inhibitor, could reverse regional contractile dysfunction and protect against adenine nucleotide loss in the “stunned myocardium”. Hearts from anesthetized dogs were “stunned” by 15 min of left anterior descending coronary artery occlusion followed by 3 hr of reperfusion. Left ventricular segment shortening (%SS) and regional myocardial blood flow (RMBF) were measured by sonomicrometry and the radioactive microsphere technique, respectively. Local coronary venous blood was withdrawn and thromboxane A 2 and prostacyclin measured by radioimmunoassay. Transmural biopsies from the reperfused and nonischemic areas were taken at 3 hr following reperfusion for tissue metabolite analysis. During ischemia, %SS, RMBF and area at risk were decreased to similar levels in both control and dazoxiben-treated hearts indicating equivalent degrees of flow deprivation. During reperfusion, %SS recovered only partially and was not significantly improved by dazoxiben. Dazoxiben augmented peak prostacyclin production (123 ± 31% vs. 292 ± 49% of preocclusion values) following reperfusion, while it completely blocked thromboxane A 2 production. Dazoxiben attenuated the decline in endocardial ATP (69 ± 5% vs. 92 ± 9% normalized to the nonischemic zone) and total adenine nucleotides. The results indicate that dazoxiben may elicit a cardioprotective effect on energy metabolism in the reperfused heart, but this is dissociated from any improvement in regional contractile function.

Myocardial Blood Flow and Oxygen Consumption during Isovolemic Hemodilution Alone and in Combination with Adenosine-Induced Controlled Hypotension

Recent reports have proposed combining isovolemic hemodilution and controlled hypotension to limit blood loss during surgery. Before such a technique can be considered for clinical use, it must be demonstrated that it does not endanger maintenance of adequate myocardial oxygenation. Accordingly, measurements of left ventricular myocardial blood flow and oxygen consumption were obtained during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension in ten pentobarbital-anesthetized, open chest dogs with normal coronary circulation. Hemodilution to a hematocrit of 21.7% was produced by isovolemic exchange of whole blood for 5% dextran. In the presence of hemodilution, adenosine was infused intravenously at a rate sufficient to decrease mean aortic pressure to 51 mm Hg. Myocardial blood flow was measured with radioactive microspheres and used to calculate global left ventricular myocardial oxygen consumption and oxygen supply. Hemodilution alone increased aortic blood flow (+43%) but had no effect on aortic pressure, left atrial pressure, heart rate, or left ventricular dP/dtmax; an increase in myocardial blood flow (+130%) maintained oxygen supply and consumption at the baseline level. Adenosine-induced hypotension during hemodilution decreased heart rate (-35%), left ventricular dP/dt max (-28%), and aortic blood flow (-14%). These systemic responses were accompanied by reduced myocardial oxygen consumption (-29%) and increased myocardial blood flow (+54%) and myocardial oxygen supply (+72%). These latter effects resulted in reduction in the coronary arteriovenous oxygen content difference and in an attendant rise in coronary sinus Po2 (+66%), which are signs of luxuriant myocardial perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

レーザー血流計による術中心筋組織血流測定法の確立と臨床応用

Recently, the technical advance of laser medicine gives us a chance to measure the myocardial blood flow.We experimentally established how to measure the myocardial blood flow using a laser flowmeter(He-Ne laser, wave length 632.8nm) and a small myocardial probe, and applied to the cases of coronary artery bypass grafting (CABG).The probe was positioned between the heart and the elastic mesh bandage (“Presnet”), and fixed on the cardiac surface. The right and left ventricular myocardial blood flow in 14 cases of CABG were counted at pre- and post-bypass grafting.The myocardial blood flow at the anterior wall of right ventricle which had no relation to bypass grafting did not change. The flow of noninfarcted bypassed region significantly(p 0.01) increased from the preoperative value of 78±12 ml/min/100gr to 87±12 ml/min/100gr after the bypass grafting.In conclusion, the noninvasive measurement of myocardial blood flow is obtained by using the laser flowmeter and the specially producted myocardial probe. The coronary artery bypass grafting increases the myocardial blood flow at the noninfarcted ischemic area.

Regional blood flows in running normotensive and renal hypertensive dogs.

The influence of short-term hypertension on the haemodynamic response to exercise was studied by measuring arterial pressure and regional blood flow (radio-active microspheres) in dogs at two levels of treadmill exercise (5 km/h at 0 degrees and 10 km/h at 4.5 degrees). One group of dogs (n = 5) had one-kidney, one clip hypertension of 1-week duration and was compared to normotensive controls (n = 5). Both groups exhibited similar increases in heart rate, but arterial pressure increased only in the normotensive dogs. Left ventricular myocardial blood flow increased significantly in both groups. However, the increase was more pronounced in the hypertensive dogs. In some groups of active skeletal muscles (biceps brachii, tibialis cranialis), increases in blood flow in excess of 30-fold were observed during exercise in normotensive animals. Several muscles showed exaggerated increases in flow in hypertensive dogs. Perfusion of the brain, the kidneys and the splanchnic area was not compromised in either group of dogs. We conclude that in one-kidney, one clip hypertension of 1-week duration, when structural cardiovascular changes are presumably far from being completely developed, vasodilatation to increased metabolic demands in the myocardium and in most skeletal muscles is not limited in response to mild to moderate levels of exercise, and that perfusion of other vascular beds is not compromised.

Silent Myocardial Ischemia and Infarction.

Part 1 Pathophysiology of silent myocardial ischaemia: cardiac pain mechanisms alterations in sensitivity to pain in patients with silent myocardial ischaemia the sequence of events during episodes of myocardial ischaemia - where does pain fit in? left ventricular dysfunction and myocardial blood flow disturbances during episodes of silent myocardial ischaemia - is less myocardium at jeopardy than during symptomatic ischaemia?. Part 2 Prevalence of asymptomatic coronary artery disease: prevalence of silent myocardial ischaemia prevalence and distinguishing features of silent myocardial infarctions. Part 3 Detection of asymptomatic coronary artery disease: what can be learned from standard diagnostic procedures? ambulatory electrocardiography (Holter monitoring) exercise testing combining the exercise test with other procedures cardiac catheterization. Part 4 Prognosis in asymptomatic coronary artery disease: prognosis in patients with silent myocardial ischaemia relation of silent myocardial ischaemia to sudden death, silent myocardial infarction and ischaemic cardiomyopathy prognosis after silent myocardial infarction and myocardial infarction without preceding angina. Part 5 Management of patients with asymptomatic coronary artery disease: medical treatment of asymptomatic coronary artery disease surgical treatment of asymptomatic coronary artery disease. Part 6 Future directions: silent myocardial ischaemia and silent myocardial infarction - what issues remain to be resolved?.

Analysis of phases of contraction during graded acute myocardial ischemia.

The quantitative effects of graded ischemia on the phases of contraction in ischemic and nonischemic myocardium were studied in 10 open-chest dogs. During progressive coronary stenosis, an index of the overall severity of ischemia, total myocardial blood flow deficit (TMFD), was measured using microspheres. Segment shortening (% delta L) during the isovolumic and ejection phases of systole in the ischemic and nonischemic zones was obtained with ultrasonic crystals. In the ischemic zone, total systolic and ejection phase % delta L decreased progressively as stenosis increased; isovolumic phase % delta L showed segment elongation (bulging) during mild ischemia, which was unchanged as ischemia became severe. Total % delta L in the nonischemic zone increased progressively with increasing stenosis, reaching 132 +/- 20% of the control value when TMFD was 24.8 +/- 6.5% of total expected left ventricular (LV) myocardial blood flow. The increase in total % delta L was entirely attributable to increased ejection % delta L and correlated with indices of preload (multivariate r = 0.65) and afterload (multivariate r = 0.62). Multiple linear regression analysis revealed that augmented contraction in the nonischemic zone was best described (multivariate r = 0.94) by a combination of four hemodynamic variables estimating LV preload and afterload, which correlated in turn with the overall severity of ischemia. Thus systolic bulging in the ischemic zone is primarily an isovolumic phase phenomenon that develops initially with mild ischemia. Little additional change occurs in the isovolumic phase as ischemic severity increases, although further reductions in shortening occur in the ejection phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise-induced cardiac hypertrophy: a correlation of blood flow and microvasculature.

The effects of exercise conditioning on the myocardium were studied in seven instrumented pigs strenuously exercised for 12 wk by treadmill running. Data were compared with eight instrumented untrained pigs. O2 consumption measured during maximum exercise effort was significantly elevated in the trained pigs (71.7 +/- 4.0 vs. 56.3 +/- 3.0 ml X ml-1 X kg-1). Absolute right and left ventricular mass increased by 20 and 13%, respectively, in response to exercise. Myocyte cross-sectional area increased by 21% in the trained hearts compared with the untrained hearts. Transmural left ventricular myocardial blood flow (ml X min-1 X g-1) was not significantly different at rest, during maximum exercise, or during exercise with adenosine infusion. However, training caused an elevation of the regional epicardial blood flow noted during exercise and exercise with adenosine. In the trained pigs mean aortic pressure during maximum exercise with adenosine infusion was not significantly different compared with untrained pigs. Coronary resistance during exercise with adenosine infusion was the same in both animal groups. In the trained group capillary numerical (no./mm2) and length (mm/mm3) densities were reduced, whereas arteriolar numerical and length densities were significantly increased compared with the untrained group. Measurements of capillary luminal surface density (mm2/mm3) in the trained group were unchanged compared with the untrained group. These results suggest that strenuous exercise does not stimulate the production of new capillaries, but this is modified by the ability of existing capillaries to increase their luminal surface area to parallel increases in myocyte growth. The arteriolar data suggest that exercise promotes the formation of new arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular mechanical efficiency in coronary artery disease

The effect of coronary artery disease and prior myocardial infarction on cardiac energetics was determined by measuring left ventricular myocardial blood flow, oxygen consumption (MVO2), efficiency and ejection phase indexes in 36 patients undergoing coronary arteriography. Eight control patients with normal coronary arteriograms and normal left ventricular function, 15 patients with coronary artery disease without prior myocardial infarction and 13 patients with coronary disease and prior myocardial infarction (greater than 6 months) were studied. Left ventricular efficiency was calculated from left ventricular work, myocardial blood flow (measured by clearance of intracoronary xenon-133), and aortic and coronary sinus oxygen content. Left ventricular volumes, mass and ejection phase indexes were measured by quantitative left ventriculography. Left ventricular myocardial blood flow per 100 g/min was reduced in patients with coronary artery disease (49.0 +/- 8; p less than 0.01) and in patients with myocardial infarction (51.6 +/- 10; p less than 0.05) compared with control subjects (62.4 +/- 16), but total left ventricular flow was not reduced because of increased left ventricular mass. As a result, MVO2 did not differ significantly for the three patient groups (control 13.3, coronary artery disease 14.0 and myocardial infarction 14.3 ml/min). In the patients with myocardial infarction, left ventricular work index was reduced (2.4 versus 4.0 kg X m/m2 per min in the control group; p less than 0.001), causing efficiency to be reduced (15.9 versus 28.8% in the control group; p less than 0.001). Decreased efficiency correlated with ejection fraction (r = 0.54), mean velocity of circumferential fiber shortening (MVcf) (r = 0.45) and mean percent chordal shortening (r = 0.43) (all p less than 0.01). These data indicate that in control patients with normal coronary arteriograms, left ventricular myocardial efficiency averages 29%; in patients with coronary disease without myocardial infarction, left ventricular MVO2 and efficiency are in the normal range; in patients with prior myocardial infarction, left ventricular efficiency is significantly reduced as a result of diminished left ventricular work and normal MVO2; and reduced efficiency after myocardial infarction correlates with reduced ejection phase indexes.

Function of mature coronary collateral vessels and cardiac performance in the exercising dog.

Formation of extensive collateral vessels after chronic constriction of a coronary artery in dogs can provide for similar increases in blood flow to native and collateralized regions of myocardium during exertion. Previous investigations have not compared myocardial blood flow and cardiac functional responses during exercise in constricted and nonconstricted (sham) animals. Thus we evaluated left ventricular performance and myocardial blood flow at rest and during mild, moderate, and severe exertion in sham-operated dogs and in dogs 2-3 mo after placement of an Ameroid occluder around the proximal left circumflex artery. Changes in double product, maximal left ventricular dP/dt, and pressure-work index were similar in both groups for each level of exertion. Despite similar increases in estimated myocardial O2 demand and similar diastolic perfusion pressures, average transmural myocardial blood flow increased less in the constrictor animals, particularly during severe exercise (2.74 +/- 0.22 vs. 1.45 +/- 0.29 ml X min-1 X g-1). The smaller increases in blood flow occurred equally in native and collateralized regions as well as in the papillary muscles and boundary areas between the native and collateralized regions. The differences in flow in the native and collateralized regions were uniform across the wall of the myocardium. We also observed smaller increases in stroke volume and cardiac output in the constrictor group, disparities which increased with increasing exertion (stroke volume, severe exercise = 0.92 +/- 0.13 vs. 0.53 +/- 0.09 ml/kg). We postulate that myocardial active hyperemia is limited either because the coronary vessels remaining after chronic circumflex occlusion cannot dilate sufficiently or that there is inappropriate active vasoconstriction during severe exertion.(ABSTRACT TRUNCATED AT 250 WORDS)