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Biomedical subjects

H Asanoi

Publications and source records attributed to H Asanoi.

At least 73 records · Page 4Linked to original sources

Pacemaker syndrome evaluated by cardiopulmonary exercise testing.

Two patients who presented with dyspnea on effort, persisting after insertion of a fixed rate ventricular demand pacemaker (VVI) for sick sinus syndrome, were evaluated by cardiopulmonary exercise testing. During VVI pacing a heightened ventilatory response to exercise and a fluctuation of ventilation occurred. The high ventilatory equivalent for CO2 throughout exercise with VVI pacing suggests that the patients had ventilation-perfusion mismatching due to an increase in the pulmonary capillary wedge pressure caused by 1:1 ventriculoatrial conduction. Rate responsive ventricular (VVIR) pacing associated with intact 1:1 ventriculoatrial conduction exaggerated the exertional dyspnea, while rate responsive atrial (AAIR) pacing improved the ventilatory response to exercise. We suggest that a heightened ventilatory response to exercise due to ventilation-perfusion mismatching may be an important factor causing the pacemaker syndrome, and that cardiopulmonary exercise testing is useful in identifying the exercise-induced symptoms with ventricular pacing.

Aged↗

Improvement of ST segment depression by gradual recruitment of collateral circulation.

The purpose of the present study was to document that the coronary collateral vessels do not open immediately upon the occurrence of myocardial ischemia. A multistage bicycle exercise was performed to determine a maximal tolerable work load until the onset of angina and significant ST segment depression in 10 patients with well-developed collateral circulation. On a different day, exercise with the maximal tolerable work load was repeated for a comparable exercise duration. In 2 of the 10 patients, anginal pain was gradually alleviated despite the continuation of exercise with fixed work load. The extent of ST segment depression at 3 min of exercise with fixed work load was 0.20 +/- 0.10 (SD) mV, significantly (p less than 0.05) greater than 0.16 +/- 0.08 mV at the end of exercise with fixed work load. In contrast, the rate-pressure product was smaller at 3 min than at the end of exercise with fixed work load (20,900 +/- 5,500 vs. 22,700 +/- 5,700 mm Hg.beats/min; p less than 0.05). In 5 patients without well-developed collateral circulation, the extent of ST depression changed in parallel with changes in rate-pressure product during exercise with fixed work load. Thus, it is concluded that the delayed collateral opening plays a critical role in the pathogenesis of myocardial ischemia in patients with a totally occluded coronary artery.

Adult↗

Development of collateral circulation after acute myocardial infarction: its role in preserving left ventricular function.

The present study evaluated the effects of coronary collateral circulation developing after acute myocardial infarction on global and regional left ventricular function during the chronic stage. The study group consisted of 16 patients with initial myocardial infarction having total occlusion of the proximal left anterior descending coronary artery. To eliminate the effects of collateral circulation existing at the onset of infarction, patients with pre-infarction angina were excluded from this study. The patients were categorized in two groups depending on the extent of their collateral circulation (collateral index: CI 0-3): group A--patients with significant collateral circulation (CI = 2 or 3) to the infarct-related coronary artery; group B--patients without significant collateral circulation (CI = 0 or 1). Their heart rate, left ventricular peak systolic and end-diastolic pressures and cardiac index were similar in the two groups. The left ventricular end-systolic volume index in the group B was significantly greater than that in the group A (60 +/- 21 ml/m2 vs 34 +/- 9 ml/m2, p less than 0.05). Left ventricular ejection fraction in the group A was significantly greater than that of the group B (55 +/- 9% vs 39 +/- 15%, p less than 0.05), and a significant difference was observed in the percentage of segment shortening in the infarct area between the groups A and B (10.8 +/- 9.2% vs -0.2 +/- 5.4%, p less than 0.01). It was concluded that coronary collateral circulation which develops after acute myocardial infarction exerts beneficial effects on global and regional left ventricular function during the chronic stage.

Adult↗

[Walk-through phenomenon by gradual recruitment of collateral circulation].

The present study was performed to investigate whether coronary collateral vessels open immediately after occurrence of myocardial ischemia. Multistage bicycle exercise was performed to determine the maximum tolerable workload until the onset of angina and significant ST segment depression in 10 patients with well-developed collateral circulation. On a different day, exercise using the maximum tolerable workload was repeated for comparable exercise durations. In two of the 10 patients, anginal pain was gradually alleviated despite the continuation of exercise using the fixed workloads. The extent of ST segment depression during three min exercise with the fixed workload was 0.20 +/- 0.10 (SD) mV, which was significantly (p less than 0.05) greater than 0.16 +/- 0.08 mV at the end of exercise with fixed workload. By contrast, the pressure-rate product was smaller at three min than at the end of exercise using the fixed workload (20,900 +/- 5,500 vs 22,700 +/- 5,700 mmHg-beats/min; p less than 0.05). It was concluded that delayed collateral openings play a critical role in the pathogenesis of the walk-through phenomenon.

Adult↗

[Ventriculo-arterial coupling during aerobic and anaerobic exercise in normal subjects].

Physiological differences in aerobic and anaerobic exercise were assessed within the coupling framework between the left ventricle and the arterial system. In 10 normal men, the anaerobic threshold was estimated using sequential breath gas analysis during incremental ergometer tests. Direct arterial pressure and left ventricular echocardiograms were simultaneously recorded as its pressure was changed by phenylephrine or nitroprusside, and the slope (Ees) and volume axis intercept (Vo) of the end-systolic pressure (ESP)-volume relationship were determined. The effective arterial elastance (Ea) was expressed by the slope of the ESP-stroke volume relationship. Assuming that the Vo was unchanged from the resting state, the Ees and Ea were determined during exercise at aerobic and anaerobic work levels for each subject. During aerobic exercise, an increase in left ventricular end-diastolic volume and the tendency to decrease in ESP caused a significant fall in Ea by 30%. There was no significant change in Ees. Consequently, Ea/Ees which correlates inversely with left ventricular pump efficiency, decreased by 35%. During anaerobic exercise, Ea remained the same as during aerobic exercise, but Ees rose substantially by 89%. This caused a further reduction in Ea/Ees (-54%). Thus, ventriculo-arterial coupling during exercise is characterized by a decrease in Ea/Ees, indicating an augmentation of pump efficiency. This is primarily mediated by changes in loading conditions (decrease in Ea) during aerobic exercise, and by enhanced contractility (increase in Ees) during anaerobic exercise.

Adult↗

Sustained inotropic effects of a new cardiotonic agent. OPC-8212 in patients with chronic heart failure.

OPC-8212, a newly synthesized noncatecholamine, nonglycosidic, orally effective inotropic agent, has been shown to exert a potent cardiotonic action in acute administration to patients with heart failure. However, its long-term effect has not yet been established. Eight patients with dilated cardiomyopathy (New York Heart Association functional class II-III) were given a single dose of 60 mg of OPC-8212 daily for 4 to 8 weeks. OPC-8212 produced symptomatic improvement in four patients. Though there were no detectable changes in arterial pressure and left ventricular end-diastolic dimension, heart rate and end-systolic dimension significantly decreased after administration of OPC-8212. Baseline fractional shortening rose significantly and depression of shortening in response to acute pressor stress (afterload mismatch) was corrected after OPC-8212. The end-systolic pressure-dimension relation was shifted to the left with a steeper slope. These findings indicate that the inotropic state was substantially enhanced by the drug. No adverse effects were observed in any patient. Thus, the drug appears to hold promise for the chronic treatment of patients with moderate congestive heart failure who are essentially asymptomatic at rest, but develop severe impairment of cardiac function in a stressed state.

Adult↗

Importance of collateral circulation for prevention of left ventricular aneurysm formation in acute myocardial infarction.

The effect of preexistent coronary collateral perfusion on the prevention of left ventricular aneurysm formation was examined in 47 patients undergoing an intracoronary thrombolysis within 6 hours after the onset of a first acute anterior myocardial infarction. Left ventricular aneurysm formation and wall motion were analyzed with cineventriculography. A left ventricular aneurysm was determined as well-defined demarcation of the infarcted segment from normally contracting myocardium. In 25 patients with successful thrombolysis (group A), a left ventricular aneurysm was observed in one patient (4%) during the chronic stage of infarction. In 10 patients who had a significant collateral circulation to the infarct-related coronary artery and unsuccessful reperfusion (group B), the left ventricular aneurysm was observed in only one patient (10%). In the remaining 12 patients with unsuccessful recanalization in the absence of a significant collateral perfusion (group C), there was a higher incidence (seven of 12, 58%) of left ventricular aneurysm formation than in groups A and B (p less than 0.05). In group A, both the global ejection fraction and regional wall motion in the infarct areas improved significantly (p less than 0.05) between the acute and chronic stages of infarction. By contrast, in groups B and C, these indexes on the ventricular function did not change significantly during the convalescent period. Thus, although the collateral perfusion existing at the onset of acute myocardial infarction may not improve ventricular function, it exerts a beneficial effect on the prevention of left ventricular aneurysm formation.

Adult↗

Ventriculoarterial coupling in normal and failing heart in humans.

To investigate coupling between the heart and arterial system in normal subjects and cardiac patients, we determined both the slope of the left ventricular end-systolic pressure-volume relation (ventricular elastance) and the slope of the arterial end-systolic pressure-stroke volume relation (effective arterial elastance) in three groups of subjects: group A, 12 subjects with ejection fraction of 60% or more; group B, seven patients with ejection fraction of 40-59%; and group C, nine patients with ejection fraction of less than 40%. We also determined the left ventricular stroke work, end-systolic potential energy, and the ventricular work efficiency defined as stroke work per pressure-volume area (stroke work + potential energy). In group A, ventricular elastance was nearly twice as large as arterial elastance. This is a condition for a maximal mechanical efficiency. In group B, ventricular elastance was almost equal to arterial elastance. This is a condition for maximal stroke work from a given end-diastolic volume. In group C, ventricular elastance was less than one half of arterial elastance, which resulted in increased potential energy and decreased work efficiency. Thus, the present study suggests that ventriculoarterial coupling is normally set toward higher left ventricular work efficiency, whereas in patients with moderate cardiac dysfunction, ventricular and arterial properties are so matched as to maximize stroke work at the expense of the work efficiency. Neither the stroke work nor the work efficiency is near maximum for patients with severe cardiac dysfunction.

Adult↗

Relationship of plasma norepinephrine to ventricular-load coupling in patients with heart failure.

The relationship of plasma norepinephrine levels to the adaptational changes in ventricular-load coupling were studied at rest and during exercise in subjects with variably depressed ventricular function. Peak body oxygen consumption (VO2) and gas exchange anaerobic threshold (ATge) were measured to assess exercise capacity. Ventricular contractile properties were expressed by the slope (Ees) of the end-systolic pressure-volume relation and mechanical arterial properties were expressed by the slope (Ea) of the end-systolic pressure-stroke volume relation. Resting plasma norepinephrine was significantly elevated in patients with severe heart failure (New York Heart Association class III, IV) and correlated well with the magnitude of reduction in peak VO2 and ATge. In these patients, Ea/Ees ratio was also increased and correlated with the levels of resting plasma norepinephrine. Although pump efficiency of the left ventricle progressively fell with the development of heart failure, stroke volume was maintained within normal range by virtue of a compensatory increase in end-diastolic volume. Sympathetic activity was much higher in anaerobic exercise than in aerobic exercise. However, Ees (ventricular contractility) remained at the same value throughout the exercise period. Thus, an increase in stroke volume during anaerobic exercise was caused more by an increase in end-diastolic volume than by an enhanced contractility. Our results suggest that the level of resting plasma norepinephrine can be a good predictor of the modulation of ventricular-load coupling in patients with heart failure and that when contractile reserve is decreased, the Frank-Starling mechanism plays an important role in the control of stroke volume.

Exercise↗

[Induction of coronary arterial spasm by intracoronary administration of acetylcholine in patients with vasospastic angina].

To examine whether intracoronary injections of acetylcholine induce coronary artery spasm in patients with vasospastic angina, incremental doses (20, 30 and 50 micrograms) were injected directly into the coronary arteries in 12 patients with variant angina (Group A: rest angina with electrocardiographic ST-segment elevation during attacks), 19 with vasospastic angina (Group B: rest angina and/or effort angina with variable threshold in the treadmill exercise stress test), 11 with organic coronary artery stenosis but without angina (Group C), and 14 without coronary artery disease (Group D). A temporary cardiac pacemaker was positioned in the right ventricle. Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in the luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in all 12 patients (100%) of Group A, in 18 (95%) of Group B, in two (18%) of Group C, and in two (14%) of Group D. Thus, the sensitivity of this method for inducing coronary spasm was 100% in group A, 95% in Group B, and 97% in Group A plus Group B. The specificity for inducing spasm was 86% in Group D, and 84% in Group C and Group D. When acetylcholine was injected separately into the left and right coronary arteries, spasm of both the coronary arteries was observed in two (40%) of Group A, in five (33%) of Group B, and none (0%) of Group C and Group D. Acetylcholine (20 micrograms) induced coronary spasm in 10 (83%) of Group A and only in nine (47%) of Group B.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

Functional characteristics of nonischemic region during pacing-induced myocardial ischemia in angina pectoris.

To investigate the details of the hyperfunction of nonischemic area during acute ischemia, the regional myocardial function at rest and immediately after rapid cardiac pacing was compared using cineventriculography in 12 patients with stable effort angina. Three left ventricular boundaries at the time of end-diastole, aortic valve opening and end-systole were superimposed, and 128 radial grids were drawn from the center of gravity of end-diastolic frame to the endocardial margin. The changes in the length of each radial grid provided quantitative description of segmental systolic function. In the ischemic area, the percent of total segment shortening decreased from 36 +/- 6% (mean +/- standard error of the mean) to 24 +/- 8% (p less than 0.05) in patients with a significant narrowing of left anterior descending coronary artery (LAD), and from 42 +/- 6% to 20 +/- 4% (p less than 0.05) in those with right coronary artery (RCA) involvement. In the nonischemic area, the percent of total segment shortening increased from 33 +/- 7% to 44 +/- 7% (p less than 0.05) in LAD disease, while it was unchanged in RCA involvement (40 +/- 5% vs 41 +/- 7%). The percentage of isovolumic segment shortening increased from 1 +/- 4% to 7 +/- 3% (p less than 0.05) and from 1 +/- 1% to 5 +/- 2% (p less than 0.05) in LAD and RCA involvement, respectively. Meanwhile, ejection phase shortening did not change significantly (33 +/- 6% vs 40 +/- 7% in LAD involvement, and 39 +/- 6% vs 38 +/- 7% in RCA involvement).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Coronary collateral development after acute myocardial infarction.

In 31 patients without a history of preinfarction angina, coronary collateral circulation to the completely obstructed coronary artery was evaluated by coronary angiography during a convalescent period of their first myocardial infarction. Collateral visualization (collateral index) was found to be significantly greater in patients with involvement of the right coronary artery (2.1 +/- 1.1, SD) than in those with obstruction of the left anterior descending coronary artery (1.2 +/- 1.0, p less than 0.05). The time interval from the onset of symptoms of acute myocardial infarction to angiographic evaluation did not affect the extent of collateral visualization or the degree of coronary artery disease. These findings indicate that the collateral vessels develop after acute myocardial infarction regardless of the extent of coronary artery disease and accomplish the proliferative process within one month. It is also suggested that the collateral visualization is dependent on the size of perfusion territory of the infarct-related coronary artery.

Angiography↗

Changes in cardiac performance after dialysis in patients with chronic renal failure.

The effect of hemodialysis on left ventricular performance in 10 uremic patients was studied utilizing echocardiography. Left ventricular function curves constructed by a lower body negative pressure method were compared before and after dialysis. Although hemodialysis caused a decrease in the stroke volume index at rest from 55 +/- 17 to 50 +/- 20 ml/m2, the left ventricular function curve did not show any detectable shift. Thus, it is concluded that a decrease in stroke volume secondary to dialysis is attributable to the reduction in preload, rather than to changes in the contractile state of the left ventricle.

Adult↗

ST-segment fluctuation during treadmill exercise in patients with angina pectoris.

The level of the ST-segment fluctuates transiently during treadmill exercise in some patients with angina pectoris. In the present study, the incidence and clinical significance of ST-segment fluctuation were studied before and after propranolol in 52 patients with angina pectoris. A transient greater than 0.5-mm (0.05 mV) upward shift of the ST-segment during a graded treadmill test was considered a significant fluctuation in leads without signs of previous myocardial infarction. The fluctuation was observed in three of 30 patients with rest or rest and effort angina pectoris before propranolol and in 14 of them after propranolol, while only one of 22 patients with effort angina alone showed fluctuation after the drug. Coronary arteriography revealed that in 15 patients showing ST-segment fluctuation with propranolol, seven patients had no significant coronary stenosis, six had one-vessel disease and two had two-vessel disease. In 24 patients with documented coronary artery spasm, ST-segment fluctuation was induced in two (8%) before propranolol and in 13 (54%) after propranolol. Our results suggest that ST-segment fluctuation during graded treadmill exercise may be related to transient coronary vasospasms exacerbated by propranolol.

Adult↗

Regional work of the human left ventricle calculated by wall stress and the natural logarithm of reciprocal of wall thickness.

Regional left ventricular work is a more precise indicator of function than is simple shortening fraction. Regional work of the ventricle normalized to a unit volume of myocardium (RWM) is given by the following equation: RWM = - intergral of sigma d[ln(1/H)], where sigma is the mean wall stress and ln(1/H) is the natural logarithm of reciprocal of wall thickness. This method has been previously validated in animal experiments and it is now extended to the clinical setting for the first time. In 10 normal subjects and 6 patients with anteroseptal myocardial infarction, ventricular minor axis and wall thickness were measured by echocardiography and recorded simultaneously with high fidelity left ventricular pressure. Then, regional work of the interventricular septum and of the posterior wall of the left ventricle was calculated from the measured pressure and dimension data. In normal subjects, regional work of the septum and posterior wall was 6.1 +/- 1.7 and 7.0 +/- 1.8 mJ/cm3, respectively; the average of the septal and posterior wall regional work multiplied by the left ventricular myocardial volume correlated well (r = 0.93) with the total mechanical work done by the entire left ventricle. In patients with anteroseptal infarction, septal regional work was greatly reduced (0.6 +/- 1.7 mJ/cm3), compared with posterior wall regional work in the same patients (6.1 +/- 1.8 mJ/cm3). This simple method can be applied clinically in assessing the functional state of different regions of the myocardium.

Adult↗

Does cytosolic free calcium concentration in platelets reflect tone and structural changes of resistance vessels?

To investigate tone and vascular changes of resistance vessels as related to cytosolic free calcium concentration [( Ca2+]i) in platelets, we measured forearm vascular resistance and free calcium concentration in platelets from 10 essential hypertensives and 15 normotensives. The [Ca2+]i in platelets was significantly higher in essential hypertensives than in normotensives (184 +/- 43 versus 146 +/- 23 nmol/l, P less than 0.01). The [Ca2+]i levels in platelets were significantly correlated with both systolic (r = 0.50, P less than 0.05) and diastolic blood pressures (r = 0.57, P less than 0.01). Resting vascular resistance and minimal vascular resistance were significantly higher in essential hypertensives than in normotensives (30.6 +/- 12.6 and 2.57 +/- 1.30 versus 16.3 +/- 8.0 and 1.47 +/- 0.63 mmHg/ml per min per 100 ml, P less than 0.05 and P less than 0.01, respectively). Both resting and minimal vascular resistance were significantly correlated with [Ca2+]i in platelets (r = 0.40 and P less than 0.05, r = 0.55 and P less than 0.01, respectively). These results suggest that [Ca2+]i in platelets reflects [Ca2+]i in vascular smooth muscle cells and may be a significant determinant of not only tone but also structural changes of resistance vessels.

Adult↗

Improvement of treadmill capacity and collateral circulation as a result of exercise with heparin pretreatment in patients with effort angina.

It has been demonstrated in animal experiments that heparin accelerates the coronary collateral development induced by repeated coronary occlusion. We used this effect of heparin for the treatment of patients with stable effort angina. In 10 patients, treadmill exercise was performed according to standard Bruce protocol twice a day for 10 days. A single intravenous dose of heparin (5000 IU) was given 10 to 20 min before each exercise period. Exercise with heparin pretreatment increased the total exercise duration from 6.3 +/- 1.9 (SD) to 9.1 +/- 2.2 min (p less than .001) and the maximal double product (DP) from 18,900 +/- 5100 to 25,500 +/- 6800 mm Hg.beats/min (p less than .001). The DP at the onset of angina was also increased by 35% (p less than .01) and the DP at which ST depression (0.1 mV) first appeared was 19% (p less than .05) greater after treatment. Repeat coronary cineangiography revealed an increase in the extent of opacification of collaterals to the jeopardized myocardium. In an additional six patients, treadmill exercise was performed with no medication twice a day for 10 days. All of the above-mentioned variables of treadmill capacity remained unchanged, despite 20 exercise periods without heparin pretreatment. Thus, heparin accelerates exercise-induced coronary collateral development by promoting angiogenesis. The development of such a therapeutic modality will open a new field for the treatment of patients with ischemia.

Angina Pectoris↗

Effect of xamoterol on myocardial energetics in man.

We analyzed the effect of xamoterol (beta 1-partial agonist) on myocardial energetics in 8 patients with normal left ventricular function. We measured resting systemic and coronary hemodynamics before and after a single intravenous injection of xamoterol (0.1 mg/kg). This agent increased heart rate from 70 +/- 7 to 80 +/- 11 beats/min (p less than 0.05) and cardiac index from 2.9 +/- 0.5 to 3.2 +/- 0.5 L/min.m2 (p less than 0.01), respectively. Left ventricular peak positive dp/dt (1870 +/- 350 vs 2620 +/- 580 mmHg/sec (p less than 0.01) and left ventricular ejection fraction (62 +/- 7 vs 70 +/- 7% (p less than 0.01] also increased, while left ventricular end-diastolic pressure (9 +/- 3 vs 5 +/- 3 mmHg (p less than 0.01] and volume index (70 +/- 14 vs 58 +/- 16 ml/m2 (p less than 0.01] decreased. Coronary blood flow and total myocardial oxygen consumption did not change significantly after intervention. As a result, xamoterol enhanced left ventricular external mechanical work versus myocardial oxygen consumption ratio (mechanical efficiency) from 20 +/- 4 to 24 +/- 5% (p less than 0.01). Myocardial oxygen extraction ratio decreased significantly (p less than 0.01) from 66 +/- 5 to 62 +/- 5% after xamoterol. We conclude that xamoterol augments left ventricular mechanical efficiency accompanied by a decrease in coronary vascular tone in patients with normal cardiac function.

Adrenergic beta-Agonists↗