Persistence of subendocardial perfusion after subtotal coronary embolisation.

The effects of acute subtotal embolisation of small coronary arteries on regional coronary flow and vasodilator reserve were investigated in seven open chest dogs. Unlabelled plastic microspheres (26(2) micron in diameter) were injected as boluses of 200,000-400,000 microspheres into the circumflex artery. Embolisation was repeated until reactive hyperaemia was totally abolished, which occurred after the injection of 62,000(4000) microspheres per gram. Intracoronary adenosine was then infused for 20 min at 1.2 mg.min-1. Regional myocardial blood flow was measured by radioactive microspheres under control conditions, after coronary embolisation, and during adenosine infusion. Coronary blood flow (0.98(0.07) ml.min-1.g-1) was reduced to 0.66(0.08) ml.min-1.g-1 after embolisation (p less than 0.005) when reactive hyperaemia was practically abolished. Embolisation reduced epicardial flow from 0.93(0.08) to 0.40(0.09) ml.min-1.g-1 (p less than 0.001), whereas endocardial flow was unchanged (1.03(0.11) vs 0.92(0.14) ml.min-1.g-1; NS); as a consequence, the endocardial to epicardial flow ratio increased from the control value of 1.11(0.06) to 2.31(0.35) (p less than 0.005). Adenosine infusion increased coronary blood flow from 0.66(0.08) to 1.66(0.41) ml.min-1.g-1 (p less than 0.05). Endocardial blood flow increased more than epicardial blood flow, leading to a further increase in the endocardial to epicardial flow ratio (3.79(0.13); p less than 0.05). Thus it is concluded that (a) embolisation of small arteries abolishes the reactive hyperaemic response to transient coronary occlusion; (b) microembolisation predominantly reduces subepicardial perfusion; and (c) adenosine administration may increase total and regional flow after subtotal occlusion of coronary small arteries.

Regional myocardial deoxyglucose uptake following electrical stimulation of canine efferent sympathetic cardiopulmonary nerves.

OBJECTIVE: The aim was to study the effect of stimulating individual acutely decentralised cardiopulmonary nerves on myocardial uptake of deoxyglucose. METHODS: In 17 open chest anaesthetised dogs the efferent axons of individual decentralised cardiopulmonary nerves were stimulated intermittently throughout 1 h while haemodynamic variables were measured. Tritiated 2-deoxyglucose was injected intravenously at the beginning of stimulation. Atropine was given when a cardiopulmonary nerve with efferent parasympathetic axons was studied. Distribution of label was detected using a multiwire proportional chamber. It was compared to blood concentration of deoxyglucose to permit quantitative mapping of regional myocardial uptake during the stimulation of each nerve. RESULTS: Neural stimulation of most of sympathetic efferent cardiopulmonary nerves increased deoxyglucose uptake in all myocardial tissue. Uptake was greatest in the left ventricle, less in the right ventricle, and least in the left and right atria. Regional myocardial uptake was also observed following individual cardiopulmonary nerve stimulation. Some nerves caused greater uptake than others. Cardiopulmonary nerves which are known to enhance inotropism when stimulated induced little increase of deoxyglucose uptake, whereas other nerves known to exert little positive inotropic effect induced considerable uptake. There was no correlation between haemodynamic changes and deoxyglucose uptake. CONCLUSIONS: It appears that (1) efferent sympathetic axons in one cardiopulmonary nerve can preferentially increase deoxyglucose uptake in specific regions of the myocardium and (2) the mechanisms responsible for enhancement of glucose uptake may differ from those responsible for inotropic responses.

Elective response to propranolol or verapamil in ischemia on effort.

Twenty-four patients with effort angina and positive exercise stress test performed four control exercise stress tests, two tests while taking propranolol (240 mg/day) and two tests while taking verapamil (320 mg/day), in a randomized crossover sequence. For each test the following parameters were measured: time and rate-pressure product at ischemia; intercept and slope of the linear regression between rate-pressure product and minutes of exercise. Group analysis showed that both drugs improved time to ischemia significantly and to the same extent. However, eight patients responded preferentially to verapamil in contrast to 12 patients on propranolol. The remaining four patients responded equally to both drugs. In verapamil responders, verapamil increased time to ischemia by decreasing intercept and increasing rate-pressure product at ischemia. In these patients, propranolol did not increase time to ischemia because of a marked decrease in rate-pressure product at ischemia. In propranolol responders the significant increase in time to ischemia during propranolol was the result of a decrease in intercept and slope. The ineffectiveness of verapamil in these patients was related to a slight decrease in intercept without any increase in rate-pressure product at ischemia. The preferential response to one of the two drugs could not be predicted on the basis of clinical and angiographic features. In conclusion, in patients with effort angina, medical treatment should be personalized and based on a direct and objective verification of a drug's efficacy since different mechanisms can modulate exercise tolerance.

Individual variability in symptoms, ischemic threshold and cardiovascular efficiency during exercise testing in patients with effort angina.

This study assessed both group and individual variability of ECG exercise stress test in patients with effort angina. Forty-five untreated patients with typical effort angina, without evidence of spontaneous angina, with a positive exercise stress test (ST depression greater than 0.2 mV) and angiographically documented coronary artery disease were studied. Four multistage exercise stress tests were performed, two in the morning and two in the afternoon, on two consecutive days. Forty-four patients completed the protocol for a total of 176 exercise stress tests. For each exercise stress test the following parameters were analyzed: time to 0.15 mV ST segment depression (time to ischemia); rate-pressure product at ischemia (ischemic threshold); slope and intercept of the linear regression between rate-pressure product and time of exercise. Silent effort ischemia was largely prevalent: 21 patients (48%) experienced chest pain in all four tests, but only seven showed a consistent time relationship between pain and ECG changes. Symptomatic patients did not appear different from the asymptomatic ones in terms of clinical and angiographic data. When group data were analyzed for each parameter the four exercise stress tests appeared reproducible. In contrast, when individual variability of each parameter was computed as the percentage difference between range (maximum--minimum) and maximal value obtained in the series of four exercise stress tests, a large variability was detected. Variability of time to ischemia, was 27.2 +/- 17.4%. This resulted from a random combination of variability in ischemic threshold (19.1 +/- 9.2%), slope (28.4 +/- 12.8%) and intercept (22.7 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Regional myocardial performance before, during and after coronary occlusion.

The effects of transient coronary occlusion upon segment length and intramyocardial pressure were studied in seven open-chest dogs. The subendocardial and subepicardial layers in the territory of the left anterior descending coronary artery were instrumented with pairs of ultrasonic crystals and miniature pressure probes. During coronary occlusion, systolic subendocardial pressure decreased from 194 +/- 11 to 141 +/- 12 mmHg (p 0.001) and systolic subepicardial pressure from 82 +/- 7 to 62 +/- 12(p 0.05). Systolic shortening was abolished in both layers. During reperfusion, systolic subendocardial pressure reached 242 +/- 22 mmHg (p 0.05) and systolic subepicardial pressure 100 +/- 10 mmHg (p 0.05). Early during reperfusion a transient overshooting was also observed in subendocardial and subepicardial systolic shortening. The observations of this study are consistent with the hypothesis that unrestricted reperfusion is associated with an overshooting in regional myocardial contractile performance.

Effect of dilazep on coronary and systemic circulations.

In order to assess the effects of dilazep on central hemodynamics and regional flows, 0.2 mg/kg of the drug were administered intravenously to 6 open-chest anesthetized dogs. Hemodynamic and flow measurements were performed under control conditions, and approximately 5, 10 and 25 min after treatment. Dilazep caused a marked and sustained reduction of coronary resistance and increased coronary blood flow. Flow increased uniformly in the subendocardial and subepicardial layers of the left ventricle so that no significant change occurred in the endo/epi flow ratio. Dilazep caused a significant reduction of total systemic resistance and aortic pressure, however flow to the liver, kidney and spleen was not reduced. We conclude that dilazep exerts a dilating action on the coronary and systemic arterial beds and increases uniformly regional myocardial blood flow. Dilazep does not alter the transmural distribution of coronary blood flow and does not impair kidney, liver and spleen perfusion.

Dipyridamole-echocardiography test as a clue for assessing the organic 'ceiling' of individual coronary reserve.

Twenty-four patients with a history of effort angina, a positive exercise stress test (EST) and coronary artery disease were enrolled in the study; 12 patients had a positive dipyridamole-echocardiography test (DET) and 12 had a negative DET. Each patient performed a total of 4 ESTs in the absence of therapy on two successive days; for each test the rate-pressure product (RPP), an established index of myocardial oxygen demand, was measured at the onset of ischaemia (ST depression greater than 0.15 mV) or at the peak of maximal exercise (if a repeated EST was negative). Taking into account the lowest of the 4 RPP values (X 1/100) in each patient, there was no significant difference between DET-negatives and DET-positives (185.2 +/- 49.3 vs 157.4 +/- 32.4). Conversely, when considering the highest of the 4 RPP values in each patient, there was a significant difference between DET-negatives and DET-positives (280.3 +/- 63.9 vs 183.3 +/- 37.0; p less than 0.01). Thus, DET may provide a clinically useful tool for assessing in the individual the organic 'ceiling' of coronary reserve, by eliminating the variability in coronary tone, which may affect EST reproducibility and the correct evaluation of the impairment of organic coronary reserve.

Regional myocardial systolic function. Effects of coronary occlusion and reperfusion.

Intramyocardial pressure and segment length were measured during control conditions, during 30 sec coronary artery occlusion, and during reperfusion in the subendocardial (ENDO) and in the subepicardial (EPI) layers of the left ventricular wall, in 9 open-chest dogs. Under control conditions systolic subendocardial pressure, 179 +/- 11 mmHg, exceeded subepicardial pressure, 97 +/- 9 mmHg (P less than .001); the maximal rate of change of pressure in the subendocardium, 2231 +/- 170 mmHg/sec, was greater than in the subepicardium, 960 +/- 125 mmHg/sec, (P less than .001). Subendocardial systolic shortening, 23 +/- 2% was greater than subepicardial systolic shortening 16 +/- 1% (P less than .001). The maximal rate of systolic shortening in the subendocardium, 32 +/- 5 mm/sec, was also higher than in the subepicardial, 14 +/- 1 mm/sec (P less than .001). When the left anterior descending coronary artery was closed, subendocardial and subepicardial systolic pressures decreased immediately; conversely, appreciable changes in segment length were delayed 10-12 heart beats. After 30 sec of coronary occlusion a 35% reduction was observed in subendocardial and subepicardial systolic pressures, and systolic lengthening occurred. During reperfusion systolic shortening showed a brief overshooting and was back to control after 10 +/- 2 sec in subepicardium and 13 +/- 2 sec in subendocardium. Systolic intramyocardial pressure recovered in 14 +/- 3 sec in EPI and 18 +/- 2 sec in ENDO and subsequently rose above control level. Peak rebound occurred after 50-75 sec of reperfusion and was 27% higher than control in subendocardium and 20% in subepicardium. In 5 dogs the effects of coronary occlusions lasting 5, 15, 30, 45 and 60 sec were investigated. A progressive increase in ischemic depression and reperfusion rebound in subendocardial and subepicardial pressures was observed. These data show that subendocardial and subepicardial are both functionally depressed by coronary occlusion and that subendocardial and subepicardial both contribute to reperfusion hyperkinesis. Systolic intramyocardial pressures persist when shortening is abolished. Ischemic depression and reperfusion rebound of systolic intramyocardial pressures are affected by duration of coronary occlusion.

Influence of selective autonomic decentralization on myocardial deoxyglucose uptake initiated by cardio-cardiac reflexes.

UNLABELLED: The aim of this study was to evaluate the effect of autonomic reflexes as initiated by stimulation of the right recurrent cardiopulmonary nerve afferent axons on myocardial deoxyglucose uptake and to determine how such uptake can be modified by selective neural ablation. The afferent axon in the right recurrent cardiopulmonary nerve was stimulated 30 s/min for 1 h in five anesthetized open-chest dogs in which 14-C labeled deoxyglucose was i.v. injected at the beginning of the stimulation period. Three additional sham-operated dogs served as neurally intact controls. Concentrations of label and glucose were measured in plasma. Regional myocardial deoxyglucose concentration was measured by quantitative autoradiography, following the calibration of plasma samples autoradiographic density by beta counting. Stimulation of right recurrent cardiopulmonary nerve afferent axons in the intact nervous system preparation did not significantly enhance deoxyglucose uptake as compared to neurally intact controls. When the right cervical vagosympathetic complex was cut a similar uptake was observed. Following decentralization of the right stellate ganglion, uptake was markedly reduced, as well as when the right cervical vagosympathetic was cut and the right stellate ganglion decentralized. CONCLUSIONS: Activation of afferent axons from cardiopulmonary receptors does not alter myocardial deoxyglucose uptake. Reduction in uptake occurs following unilateral stellate ganglion decentralization.