Heart Rate-systolic Pressure Product Research Articles

Umbilical cord vitamin D, ionized calcium and myocardial oxygen demand

Objective: Systemic blood vitamin D and total calcium are correlates of birthweight and cardiovascular disease but whether umbilical cord blood vitamin D and ionized calcium are correlates of birthweight and cardiovascular function is not known. This cross-sectional study correlates umbilical cord vitamin D, ionized calcium and birthweight with the heart rate-systolic pressure product (RPP), an indicator of myocardial oxygen demand.Methods: Cord blood vitamin D and ionized calcium concentrations were compared for vitamin D normal (≥50 nM, 20 ng/mL) and vitamin D deficiency (<50 nM, 20 ng/mL) in normal weight (≥2500 g) and low birthweight (LBW, <2500 g) newborns. Heart rate and blood pressure were measured during postnatal transition and RPP was computed.Results: RPP was positively correlated with birthweight (r = +0.52, p < 0.001) and with cord ionized calcium level (r = +0.42, p < 0.01) in the normal and LBW newborns. RPP was positively correlated with cord vitamin D level in the LBW newborns (raw r = +0.50, p < 0.05, normalized for birthweight r = +0.73, p < 0.01).Conclusions: Small RPP, an indicator of low myocardial oxygen demand, in LBW newborns appears to correlate with low umbilical cord vitamin D and ionized calcium levels, suggestive of pathological heart development.

Oxygen Consumption at 30 W of Exercise Is Surrogate for Peak Oxygen Consumption in Evaluation of Cardiorespiratory Fitness in Young-Adult African-American Females

Body mass index (BMI) is negatively correlated with cardiorespiratory fitness, measured by maximal or peak oxygen consumption (VO2peak). VO2peak measurements require heavy aerobic exercise to near exhaustion which increases the potential for adverse cardiovascular events. This study tests the hypothesis that VO2 measured at a fixed submaximal workload of 30 W is a surrogate for VO2peak. We studied 42 normotensive African-American female university students, 18–25 years of age. We measured VO2peak, blood pressure, and VO2 at a 30 W exercise workload and computed BMI. We found significant negative correlations between BMI and VO2peak (r = −0.41, P < 0.01) and between BMI and VO2 at 30 W (r = −0.53, P < 0.001). Compared to VO2peak, VO2 at 30 W increased the significance of the negative correlation with BMI. The heart rate-systolic pressure product at 30 W was positively correlated with BMI (r = 0.36, P < 0.01) and negatively correlated with VO2peak (r = −0.38, P < 0.001). The positive correlation between BMI and the heart rate-systolic pressure product and the greater negative correlation between VO2 and BMI at 30 W of exercise than that at exercise to fatigue suggest that normalized measurements of VO2 at the fixed exercise workload of 30 W could be useful surrogates for measurements of VO2peak.

Effects of Dietary Nitrates on Systemic and Cerebrovascular Hemodynamics

Cerebral blood flow dysregulation is often associated with hypertension. We hypothesized that a beetroot juice (BRJ) treatment could decrease blood pressure and cerebrovascular resistance (CVR). We subjected 12 healthy females to control and BRJ treatments. Cerebrovascular resistance index (CVRI), systolic blood pressure (SBP), total vascular resistance (TVR), and the heart rate-systolic pressure product (RPP) measured at rest and at two exercise workloads were lower after the BRJ treatment. CVRI, SBP, and RPP were lower without a lower TVR at the highest exercise level. These findings suggest improved systemic and cerebral hemodynamics that could translate into a dietary treatment for hypertension.

Orthostatic intolerance and coronary reserve: a matter of a certain gravity

A 74-year-old woman came to our attention complaining of the recent onset of shortness of breath during light physical activity. She reported orthostatic light-headedness, occasional dizziness, and pre-syncope symptoms for a duration of the prior year. The past history included mitral valve prolapse with mild regurgitation, dyslipidemia, and paroxysmal atrial fibrillation. At presentation, the current medications included propafenone, aminosalicylic acid, and simvastatin. A 24-h-ECG demonstrated the presence of polymorphic ventricular premature beats and asymptomatic ST-segment depression. The treadmill exercise test showed limited exercise tolerance, and a significant downward sloping ST-segment depression in leads V4–V6 at the beginning of step 2 of the Bruce protocol. An exercise myocardial perfusion scan was consistent with a reduced coronary reserve of the anterior wall. Upon admission, lying and up-right arterial pressures were 130/80 and 90/50 mmHg, respectively, while a physical examination documented a systolic click and a late systolic murmur. After medications were suspended, a new treadmill exercise test (Fig. 1, left panel) demonstrated orthostatic hypotension [1] with tachycardia upon standing, and a further decline of arterial pressure and heart rate increase during the Bruce stage 1. Exercise was interrupted due to pre-syncope symptoms after 204600 when 88% of the predicted maximal heart rate had been reached, and ST depression (-1.0 mm, V5–V6) observed. Considering the patient’s characteristics, the estimated pre-test probability of a significant coronary stenosis was 20–50% [2, 3]. The positive likelihood ratio of exercise stress test and myocardial perfusion scan for a significant coronary artery disease was about 10[4]. Thus, the patient’s post-test probability of a significant coronary stenosis was in the 70–90% range. A coronary angiography was thus performed, but ruled out a stenosis of the major coronary vessels. In the absence of stenosis, a reduction of coronary reserve may be secondary to functional mechanisms [5], including the originally misdiagnosed orthostatic hypotension. We thus hypothesized a critical decline in coronary blood flow during upright physical activity due to an exercise-induced significant decrease in arterial pressure on a pre-existing orthostatic hypotension background. To test our hypothesis, an exercise bicycle test was performed in the lying posture, a position unlikely to affect arterial pressure. Exercise was interrupted at 703500 because of physical exhaustion (Fig. 1, right panel). Neither a significant reduction in arterial pressure nor ST-segment changes was observed along the exercise-induced heart rate increase. The maximum heart rate systolic pressure product [6], a broad index of cardiovascular function, increased more when exercise was performed in a lying position than during up-right posture, compared to baseline, although the increase in heart rate was lower in the supine than in the standing position (Fig. 1). G. Costantino Medicina Interna II, Ospedale Sacco, Milan, Italy

Curative effect of Nifedipine Sustained to hypertension accompanies stabilily angina pectoris

Objective The discussion Nifedipine Sustained to treat hypertension partner stable angina pectoris the clinical curative effect. Method To conforms to hyperten-sion partner stable angina pectoris diagnosis standard patient to divide into two groups stochastically, the treatment group gives; NifedipineSustained The control group gives Captropile, observes two group of patient's blood pressure, the angina pectoris outbreak situation and the main cardiovascular event formation rate. Result The treatment group and control group voltage dropping resistor effectiveness respectively are 93.3% and 90% (P>0.05), non-significance difference: But the angina pectoris outbreak number of times and the outbreak duration, the total movement time, ST pull down lead the association number, the heart rate systolic pressure product, the movement sincere and truthful heart colic outbreak time or the ST section pull down ≥1mm comparison obviously, the curative effect (P<0.05).Conclusion NifedipineSustained to be able effective voltage dropping resistor, improvement stable angina pectoris patient's symptom and movement ability. Key words: IfedipineSustained; Captropile; Hypertension; angina pectoris

Impaired myocardial oxidative metabolism in the remote normal region in patients in the chronic phase of myocardial infarction and left ventricular remodeling

BackgroundLeft ventricular (LV) remodeling occurs in the remote normal region in the LVs after myocardial infarction (MI) and is closely involved in heart failure. MethodsWe assessed myocardial oxygen consumption using a clearance rate constant Kmono for the time activity curves of 11C-acetate in 15 patients with a prior anterior wall MI, 8 with a prior inferior wall MI, and 10 age-matched normal control subjects. LV end-systolic volume index (ESVI) was determined by echocardiography. ResultsThe LVESVI was significantly greater in patients with an anterior and inferior MI than in control subjects. The heart rate systolic pressure product did not differ among the groups. Kmono in the remote normal region in patients with an anterior MI was significantly less than that in the corresponding area in control subjects (0.055 ± 0.005 vs 0.065 ± 0.008 min−1, P < .001). Kmono in the remote normal region in those with an inferior MI was also significantly less compared with controls (0.054 ± 0.007 vs 0.069 ± 0.010 min−1, P < .01). ConclusionIn patients with a prior MI and LV remodeling, myocardial oxidative metabolism is apparently impaired in the remote normal region where augmented myocardial energy production is needed against the increased end-systolic wall stress caused by LV dilatation.

What induces the warm-up ischemia/angina phenomenon: exercise or myocardial ischemia?

The relation of the warm-up ischemia phenomenon to the presence and intensity of initial myocardial ischemia is unclear. We sought to determine whether the warm-up ischemia phenomenon requires initial myocardial ischemia or can be induced by exercise without ischemia and whether there is a relation between the intensity of initial ischemia and the attenuation of ischemia on reexercise. Twelve subjects with exertional myocardial ischemia performed 2 exercise ECG tests (1 and 2) at a +/-10-minute interval on 3 occasions (A, B, C) 1 month apart. A1 and A2 were symptom-limited. B1 was kept as long as A1, but its intensity was held under the ischemic threshold (heart ratexsystolic pressure at 1-mm ST depression [STD]) noted at A1. B2 was symptom-limited. C1 was also kept as long as A1 but with an intensity adjusted to maintain one-half maximum STD of A1. C2 was symptom-limited. Exercise duration of A2, B2, and C2 increased similarly compared with A1 (P=0.009). However, the ischemic threshold (x10-3) increased at A2 (23.5+/-6.0) compared with A1 (20.3+/-4.8; P<0.0001) but not at B2 (19.8+/-5.0) or C2 (21.5+/-5.8). Similarly, maximum STD adjusted to the highest heart rate-systolic pressure product common to A1, A2, B2, and C2 decreased at A2 (1.4+/-0.7 mm) compared with A1 (2.5+/-0.9 mm; P<0.0001) but not at B2 (2.7+/-0.9 mm) or C2 (2.3+/-0.9 mm). Exercises under the ischemic threshold and of intermediate ischemic intensity increase short-term exercise capacity, but myocardial ischemia of more than moderate intensity is needed to induce the warm-up ischemia phenomenon.

Effect of massive sympathetic nervous system activation on coronary blood flow and myocardial energy pool.

Our previous work indicates that myocardial ischemia could be the mechanism responsible for the left ventricular (LV) dysfunction that frequently develops after massive sympathetic nervous system (SNS) activation. In this study, coronary blood flow (CBF) and myocardial ATP, creatine phosphate, and lactate concentrations were measured after massively activating the SNS of anesthetized rabbits with an intracisternal injection of veratrine. CBF was measured at time 0 (baseline), and at 2, 10, and 20 min after SNS activation in one group, and at 0, 45, 90, and 150 min in a second group. Myocardial ATP, creatine phosphate, and lactate were measured at 0, 2, 10, 20, 90, and 150 min in separate groups of rabbits. SNS activation caused LV dysfunction in approximately 60% of the rabbits. SNS-related increases in CBF kept pace with the increases in myocardial energy demand as determined from the systolic pressure-heart rate product. The subendocardial-to-subepicardial blood flow ratio did not change significantly. Myocardial creatine phosphate concentration was depressed 2 min after SNS activation and remained depressed for at least 20 min. ATP fell continuously and was significantly lower than baseline by 20 min. Tissue lactate concentration was elevated at this time. By 90 min, the concentrations of all three metabolites had recovered. These results indicate that myocardial high-energy phosphate compounds fall after massive SNS activation, but ischemia does not appear to be the underlying mechanism.

Effects of the repeated administration of adenosine and heparin on myocardial perfusion in patients with chronic stable angina pectoris

The mechanism by which ischemia stimulates angiogenesis is unknown. Adenosine is released during myocardial ischemia and may be a mediator of this process. Experimental data suggest that heparin may enhance this effect. The purpose of this open-labeled, placebo-controlled trial was to determine whether repeated intravenous administration of adenosine and heparin could mimic physiologic angiogenesis and reduce the amount of exercise-induced myocardial ischemia in patients with coronary artery disease. Subjects with chronic stable angina refractory to conventional medical therapy and not suitable for revascularization received either adenosine (140 μg/kg/min for 6 minutes) and heparin (10,000 U bolus), (n = 14), or placebo, (n = 7) daily for 10 days. All patients underwent baseline and follow-up exercise testing with thallium-201 single-photon emission computed tomography myocardial perfusion imaging. A semiquantitative assessment of the extent and severity of the perfusion abnormalities was calculated by 2 blinded investigators. There was no significant change in exercise duration or in the peak heart rate systolic blood pressure product associated with adenosine and heparin compared with placebo treatment. There was, however, a 9% reduction in the extent (60.6 ± 4.0 vs 54.9 ± 4.1, p = 0.03) and a 14% improvement in severity (41.5 ± 3.2 vs 35.7 ± 2.9, p = 0.01) of the myocardial perfusion abnormalities seen in patients who received adenosine and heparin compared with placebo. Thus, in this pilot study, repeated administration of adenosine and heparin reduced the amount of exercise-induced ischemia in patients with chronic stable angina refractory to conventional treatment.

Inhibition of glycolysis and enhanced mechanical function of working rat hearts as a result of adenosine A1 receptor stimulation during reperfusion following ischaemia.

1. This study examined effects of adenosine and selective adenosine A1 and A2 receptor agonists on glucose metabolism in rat isolated working hearts perfused under aerobic conditions and during reperfusion after 35 min of global no-flow ischaemia. 2. Hearts were perfused with a modified Krebs-Henseleit buffer containing 1.25 mM Ca2+, 11 mM glucose, 1.2 mM palmitate and insulin (100 muu ml-1), and paced at 280 beats min-1. Rates of glycolysis and glucose oxidation were measured from the quantitative production of 3H2O and 14CO2, respectively, from [5-3H/U-14C]-glucose. 3. Under aerobic conditions, adenosine (100 microM) and the adenosine A1 receptor agonist, N6-cyclohexyladenosine (CHA, 0.05 microM), inhibited glycolysis but had no effect on either glucose oxidation or mechanical function (as assessed by heart rate systolic pressure product). The improved coupling of glycolysis to glucose oxidation reduced the calculated rate of proton production from glucose metabolism. The adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX 0.3 microM) did not alter glycolysis or glucose oxidation per se but completely antagonized the adenosine- and CHA-induced inhibition of glycolysis and proton production. 4. During aerobic reperfusion following ischaemia, CHA (0.05 microM) again inhibited glycolysis and proton production from glucose metabolism and had no effect on glucose oxidation. CHA also significantly enhanced the recovery of mechanical function. In contrast, the selective adenosine A2a receptor agonist, CGS-21680 (1.0 microM), exerted no metabolic or mechanical effects. Similar profiles of action were seen if these agonists were present during ischaemia and throughout reperfusion or when they were present only during reperfusion. 5. DPCPX (0.3 microM), added at reperfusion, antagonized the CHA-induced improvement in mechanical function. It also significantly depressed the recovery of mechanical function per se during reperfusion. Both the metabolic and mechanical effects of adenosine (100 microM) were antagonized by the nonselective A1/A2 antagonist, 8-sulphophenyltheophylline (100 microM). 6. These data demonstrate that inhibition of glycolysis and improved recovery of mechanical function during reperfusion of rat isolated hearts are mediated by an adenosine A1 receptor mechanism. Improved coupling of glycolysis and glucose oxidation during reperfusion may contribute to the enhanced recovery of mechanical function by decreasing proton production from glucose metabolism and the potential for intracellular Ca2+ accumulation, which if not corrected leads to mechanical dysfunction of the postischaemic myocardium.

Synergism between prostaglandin E2 and isoproterenol in stimulating glucose oxidation in the heart.

The increase in cardiac contractile function following adrenergic stimulation is accompanied by increased glucose metabolism. Since prostaglandin E2 (PGE2) can internalize beta-receptors, we determined what effects PGE2 and isoproterenol have on glycolysis and glucose oxidation in the isolated working rat heart. All hearts were perfused with Krebs-Henseleit buffer containing 11 mM [5-3H, 14C(U)]glucose, 100 microU/mL insulin, and 3% albumin. In the presence of 0.4 mM palmitate and 1.25 mM free Ca2+, isoproterenol (3 x 10(-8) M) increased the heart rate x peak systolic pressure product from 27 +/- 1 to 43 +/- 1 mmHg.beats.min-1.10(3) (1 mmHg = 133.3 Pa). This was accompanied by an increase in glycolytic rates from 3564 +/- 231 to 7775 +/- 475 nmol.g-1 dry weight min-1 and an increase in glucose oxidation from 930 +/- 72 to 2591 +/- 239 nmol.g-1 dry weight.min-1. Addition of PGE2 (10(-9) M) did not affect the isoproterenol stimulation of glycolysis, but caused a further increase in glucose oxidation (to 3863 +/- 495 nmol.g-1 dry weight.min-1). In the absence of isoproterenol, 10(-9) M PGE2 had no effect on either glycolysis or glucose oxidation. When perfusate [Ca2+] was raised to 2.5 mM, a significant increase in glycolysis was seen in control hearts (from 3564 +/- 231 to 5679 +/- 374 nmol.g-1 dry weight.min-1). The effects of isoproterenol and PGE2 on glucose metabolism remained, although the synergistic effects of PGE2 on glucose oxidation were less dramatic. When 1.2 mM palmitate was present in hearts perfused with 2.5 mM Ca2+, a decrease was seen in both glycolysis (from 5679 +/- 374 to 3027 +/- 346 nmol.g-1 dry weight.min-1) and glucose oxidation (from 1056 +/- 170 to 221 +/- 29 nmol.g-1 dry weight.min-1). Even at this high concentration of fatty acid, isoproterenol stimulated glucose oxidation (from 221 +/- 29 to 859 +/- 69 nmol.g-1 dry weight min-1), and addition of PGE2 resulted in a significant further increase (1021 +/- 139 nmol.g-1 dry weight.min-1). These data demonstrate that concentrations of PGE2 that bind to the high affinity cardiac PGE2 receptor have no effect on glucose metabolism in the absence of beta-agonists. In the presence of isoproterenol, which dramatically stimulates both glycolysis and glucose oxidation, PGE2 has a synergistic effect on glucose oxidation at lower fatty acid concentrations. These findings suggest that PGE2 receptors in the heart function to potentiate rather than decrease beta-adrenergic stimulation of glucose metabolism.

Effects of intravenous ethanol on diameter of epicardial coronary arteries

T here is controversy concerning the effects of ethanol on the coronary vasculature. In animals, ethanol causes inte;lse coronary arterial vasoconstriction.‘,2 In contrast, in man, intracoronary ethanol increases coronary blood flow without changing epicardial coronary arterial dimensions, presumably by dilating the small resistance vessels.3 Because of these conflicting results, we performed this study to assess the influence of intravenous ethanol on heart rate, systemic arterial pressure, and epicardial coronary arterial dimensions in humans. . . . We studied 16 patients (13 men and 3 women, aged 37 to 67 years) undergoing cardiac catheterization for the evaluation of chest pain. The protocol was approved by the Human Subjects Review Committee of the University of Texas Southwestern Medical Center, and all patients gave written, informed consent. No subject had a previous or ongoing problem with alcohol abuse. Antianginal medications were discontinued for >12 hours before the study; no patient smoked for >3 hours before study. All patients were studied in the fasting state after premeditation with oral diazepam 5 to 10 mg. An 8Fr sheath was inserted percutaneously in the femoral artery, through which a Judkins catheter was advanced to the ostium of the left coronary artery. Systemic arterial pressure was measured through the catheter, and heart rate was determined electrocardiographically. The heart rate-systolic arterial pressure product was used as an estimate of myocardial oxygen demand.4 An initial cineangiogram was performed to exclude narrowing of the left main coronary artery. Provided that

The patient with coronary heart disease at altitude: observations during acute exposure to 3100 meters

Nine men with documented coronary artery disease who had exercise-induced angina and/or ST segment depression were studied by treadmill testing at 1600 m and during acute exposure to 3100 m altitude. Mean maximal oxygen uptake was reduced at altitude by 11% (range, 5–26%). Ventilation, heart rate, and systolic pressure at submaximal workloads were increased at 3100 m, but maximal values were unchanged. Oxygen saturation was reduced at rest, and during submaximal and maximal exercise (88.3 ± 14 vs 93.4 ± 0.7%). Angina and/or ST segment depression occurred at the same heart rate systolic pressure product, but at lower workloads. Systolic time intervals were unchanged at altitude. A target heart rate range of 70–85% of the ischemic end-point rate at lower altitude predicted an appropriate level of tolerable exercise at high altitude. We conclude that activity prescription for coronary patients with angina on arrival at high altitude should be based on heart rate rather than workload.

Comparison of antianginal efficacies and exercise hemodynamic effects of nifedipine and diltiazem in stable angina pectoris

The antianginal efficacies of nifedipine (40 to 120 mg/day) and diltiazem (120 to 360 mg/day) were studied in 21 normotensive patients with chronic stable angina pectoris, using a randomized, double-blind, crossover design. Patients received each agent titrated to maximum tolerated doses for 6 weeks, after a 2-week placebo baseline period. The maximum tolerated dose for nifedipine was 72 ± 8 (standard error) mg/day and for diltiazem 297 ±20 mg/day. Two patients discontinued nifedipine early because of side effects. Duration of symptom-limited treadmill exercise was longer during the nifedipine (556 ± 43 seconds) and diltiazem periods (546 ± 39 seconds) compared with placebo baseline (474 ± 41 seconds, p < 0.02). Compared with placebo, nifedipine caused a significant increase in heart rate both at rest standing and at peak exercise. Nifedipine decreased resting systolic blood pressure but had no effect at peak exercise. In contrast, diltiazem caused a significant decrease in heart rate at rest but had no effect on blood pressure at rest or at peak exercise. Thus, nifedipine and diltiazem have differential effects on heart rate and systolic blood pressure suggesting different modes of action. However, despite the increase in exercise duration, neither nifedipine nor diltiazem increased the heart rate-systolic pressure product during maximum exercise. This suggests that the antianginal effects of the 2 agents probably are mediated via reduction of myocardial oxygen demand at submaximal exercise. In addition, diltiazem appears to be better tolerated than nifedipine.

Reversal of chronic ischemic myocardial dysfunction after transluminal coronary angioplasty

From a cohort of patients referred for elective transluminal coronary angioplasty, a subset of patients was evaluated to determine whether revascularization using coronary angioplasty could salvage chronically ischemic myocardium. Reversible chronic ischemic left ventricular dysfunction was identified by a severe wall motion abnormality at rest and at least one of the following: 1) persistent angina pectoris; 2) postextrasystolic ventricular contraction potentiation of motion in the asynergic zone on baseline ventriculogram; and 3) thallium-201 uptake in the asynergic zone. Twelve patients were identified as having reversible chronic ischemia and underwent coronary angioplasty. Their mean age was 63 ± 11 years and duration of symptoms 8.3 ± 9.7 weeks. Immediate pre- and postangioplasty left ventriculograms were obtained. Regional wall motion was analyzed using a radial axis model, and global ejection fraction was calculated.After angioplasty, tension development (heart ratesystolic pressure product) increased in the absence of an increase in left ventricular end-diastolic pressure. Global ejection fraction increased from 46 ± 20 to 62 ± 19% (p < 0.005). The percent of left ventricular diastolic perimeter showing asynergy decreased from 29 ± 11 to 10 ± 13% (p < 0.005). During follow-up ranging from 6 to 51 months, sudden death occurred in one patient who had had no improvement in wall motion after angioplasty, repeat angioplasty was performed in three patients and eight patients remained asymptomatic.Application of easily obtainable clinical data identifies a subset of patients with chronically ischemic myocardium. Coronary angioplasty in such patients is useful in salvaging hibernating myocardium.

Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms. 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exerciseinduced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood ramples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method).The mean baseline beta-eadorphin plasma level was 22.5 ± 19 pg/ml in patients with anginal symptoms compared with 43.7 ± 28 pg/ml in asymptomatic patients (p < 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups, Group II patients had a longer exercise duration p < 0.01), more pronounced ST segment depression (p < 0.001) and a higher peak rate-pressure product (p < 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups.These data suggest that higher baseline bata-endorphin plasma levels may play a role in the decreased sensitevity to pain in patients with slient myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.

Coronary and cardiac responses to exercise after chronic ventricular sympathectomy.

This study examined the effects of chronic surgical ventricular sympathectomy on the relationships between left ventricular mechanical performance, coronary blood flow, and exercise workload in sham-operated control dogs and dogs which had been ventricular sympathectomized 8 wk earlier. During exercise, left ventricular global contractile state was less in sympathectomized ventricles than in control ventricles, as indicated by reduced systolic pressure and maximal rate of pressure generation. Regional contractile shortening was not different. Heart rate was significantly elevated in sympathectomized ventricles. Therefore, peak systolic pressure-heart rate product and tension-time index were not different in sympathectomized ventricles compared to control ventricles. However, at each level of exercise, mean coronary flow in sympathectomized ventricles was reduced by about 50% compared to control values. The slopes of coronary flow on pressure-rate product and tension-time index were also reduced. No difference in left ventricular oxygen extraction between control and sympathectomized hearts were observed. Thus, chronic ventricular sympathectomy altered the relationships between coronary flow and oxygen consumption, on the one hand, and ventricular oxygen-dependent performance and whole-body exercise level, on the other hand.

Determinants of infarct size during permanent occlusion of a coronary artery in the closed chest dog

One hundred nine dogs subjected to experienced experimental coronary occlusion were retrospectively examined in an attempt to identify factors influencing infarct size. A coronary artery was occluded by an embolus. The field of the occluded artery (zone at risk) was determined by subsequent autoradiography of 141-cerium-labeled microspheres that were injected into the left ventricle 2 minutes after embolization. Fifty-eight dogs were analyzed after 24 hours of embolization and 51 after 48 hours. Infarct size (assessed by tetrazolium staining) was directly proportional to the size of the zone at risk in both groups. The percent of the risk zone that developed infarction was independent of risk zone size in both the 24 and 48 hour groups. No differences were seen between male and female animals or between the dogs with left circumflex or left anterior descending artery occlusion. Infarct size was also independent of the heart rate-systolic pressure product at the time of coronary occlusion, and of the time of year. Eighty percent of the variability in the portion of the risk zone that infarcted in this population could be explained by the level of collateral flow in the risk zone 2 minutes after embolization. The linear regression between the percent of the risk zone that developed infarction and collateral flow was the same in slope and intercept between the 24 and 48 hour groups. The correlation between infarct size and collateral flow was slightly better when collateral flow was expressed as a percent of flow in the nonischemic zone than when it was expressed in absolute terms.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical significance of exercise-induced silent myocardial ischemia in patients with coronary artery disease

Exercise-induced silent myocardial ischemia is a frequent feature in patients with coronary artery disease. The purpose of this study was to compare the clinical and angiographic characteristics of 269 patients who complained of chest pain during an exercise test (group I) with those of 204 who developed exercise-induced silent myocardial ischemia (group II). Group I patients more frequently had anginal symptoms of class III and IV of the Canadian Cardiovascular Society than did group II patients, who had milder symptoms (p less than 0.001). The only angiographic difference observed between the two groups was a slightly but significantly higher left ventricular end-diastolic pressure in group II patients (p less than 0.05), who also showed a longer exercise duration (p less than 0.01) with a higher heart rate-systolic pressure product (p less than 0.01) and more pronounced ST segment depression at peak exercise (p less than 0.001). Moreover, ventricular ectopic beats during exercise were more frequently observed in group II patients (p less than 0.05). Coronary bypass surgery was performed in 45% of patients of group I and in 24% of patients of group II (p less than 0.05). Survival curves of medically treated patients did not show any statistically significant difference between the two groups. Thus, although patients with a defective anginal warning system may have more pronounced signs of myocardial ischemia and a greater incidence of ventricular arrhythmias during exercise, their long-term prognosis is not different from that of patients who are stopped by angina from the activity that is inducing myocardial ischemia.

Comparative Effects of Nicorandil, Nitroglycerin, Nicotinic Acid, and SG-86 on the Metabolic Status and Functional Recovery of the Ischemic-Reperfused Myocardium

The effects of nicorandil (SG-75), its major metabolite (SG-86), nitroglycerin, and nicotinic acid on myocardial segment shortening (% SS) and velocity of shortening (dL/dt, mm/s) were compared with those of a control group during 15 min of coronary occlusion followed by 3 h of reperfusion in anesthetized dogs. Piezoelectric crystals were used to measure % SS and dL/dt in regions perfused by the left anterior descending (LAD) and left circumflex (LC) coronary arteries. The radioactive microsphere technique was used to measure regional myocardial blood flow, and arterial and coronary sinus blood samples were obtained for the determination of glucose and free fatty acids. All drugs were administered intravenously 30 min before and throughout the occlusion period. Nicorandil (25 micrograms/kg/min) and nitroglycerin (3 micrograms/kg/min) produced nearly equivalent reductions in the heart rate-systolic pressure product. Nicotinic acid (0.3 mg/kg/min) and SG-86 (50 micrograms/kg/min) had no hemodynamic effects. Nicotinic acid reduced free fatty acid uptake during occlusion and at 30 min of reperfusion, whereas the other three agents had no major effects on substrate utilization. During occlusion, % SS in the ischemic region was severely depressed; collateral blood flow was similar in each series. However, during reperfusion, the nicorandil- and nicotinic acid-treated animals showed a marked improvement in % SS and dL/dt, as compared with those treated with saline (control), nitroglycerin, or SG-86. The mechanism(s) responsible for the beneficial actions of nicotinic acid and nicorandil in this model are unknown but may be partially related to the effect of nicotinic acid to reduce fatty acid uptake by the ischemic myocardium and the peripheral hemodynamic actions of nicorandil.