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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 19 recordsLinked to original sources
PubMed1998

Thoracic spinal neuron responses to repeated myocardial ischemia and epicardial bradykinin.

Bradykinin has been strongly implicated as a mediator of cardiac nociception. During coronary artery occlusion, the content of bradykinin in coronary sinus blood increases. In non-cardiac tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rigorously studied in the heart. This raises the question that repeated coronary occlusions may also result in tachyphylaxis, thereby reducing cardiac sensation on subsequent ischemic stimulation. We therefore examined the hypothesis that repetitive episodes of myocardial ischemia and of epicardial application of bradykinin demonstrate tachyphylaxis. Mongrel cats were anesthetized with alpha-chloralose and heart rate, arterial pressure, and thoracic spinal neuron firing rate were recorded during 60 s of anterior descending coronary occlusion or local epicardial application of bradykinin (10 microM). Neurons were identified by cutaneous receptive fields in the left shoulder area. Sixty-one of 93 neurons tested responded with an increase in firing rate to coronary artery occlusion only (n=24), bradykinin only (n=19) or to both (n=18). On repetitive coronary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykinin (p<0.05). Similar responses were observed in thoracic spinal neurons that projected to the brain. In neurons demonstrating tachyphylaxis, dorsal cervical cold block partially restored the neuronal activation to coronary occlusion but not to bradykinin. We conclude, based on neuronal responses to repetitive stimuli, that afferent spinal responses to coronary occlusion and bradykinin are different. These data suggest that bradykinin is not the sole mediator of myocardial ischemic pain. The tachyphylaxis to repeated coronary artery occlusions may contribute to the clinical phenomenon of silent myocardial ischemia.

Animals↗
PubMed1996

White adipose tissue nitric oxide synthase: a potential source for NO production.

Nitric oxide synthase (NOS) activity was detected in soluble and membranous fractions of adipose tissue homogenates of control rats. After LPS-treatment, this activity was (i) markedly increased (about 10-fold) in both fractions, (ii) unaltered after dexamethasone pretreatment, (iii) partly calcium-calmodulin sensitive, and (iv) almost entirely accounted by the NOS activity found in isolated adipocytes. In adipose tissue homogenates from control rats, Western blot analysis demonstrated the presence of the endothelial (eNOS) isoform in the membranous fraction of control rats and of the inducible (iNOS) isoform in the soluble and membranous fractions. After LPS treatment, the amount of immunoreactive iNOS protein was dramatically increased, suggesting that adipose tissue is an important site of NO production during the endotoxic shock.

Adipose Tissue↗
PubMed1995

Can atherosclerotic coronary arteries vasodilate? An intraoperative high-frequency epicardial echocardiographic study.

Our purpose was to evaluate the vasodilating responses of atherosclerotic coronary arteries using intraoperative high-frequency (12 MHz) epicardial echocardiography. We obtained continuous high-frequency epicardial echocardiographic recordings during surgery, and determined cross-sectional lumen area from 17 coronary arterial segments (12 patients). Nitroglycerin (100 to 400 micrograms/min) was administered intravenously to reduce mean (+/- SEM) arterial pressure 14 +/- 1.8 mm Hg. The cross-sectional arterial images were classified using 3 different parameters: arterial lumen area, percentage of the arterial wall circumference that was atherosclerotic (wall thickness > 0.7 mm), and presence of an eccentrically shaped arterial lumen (maximal/minimal luminal diameter > 1.5). Nine arterial segments had small (< 5.0 mm2) arterial lumens (1.7 +/- 0.40 mm2 [+/- SEM; range 0.6 to 3.9]). With nitroglycerin, the luminal area increased 0.8 +/- 0.28 mm2 (range 0 to 2.5), and 39 +/- 12.1% (range 0 to 117). The remaining 8 segments had larger (> 5.0 mm2) lumens (8.7 +/- 0.91 mm2 [range 5.0 to 11.9]). With nitroglycerin the luminal area increased 4.3 +/- 1.11 mm2 (range 1.4 to 11.4), and 51 +/- 10.2% (range 16 to 96). Seven arterial segments had eccentric lumens; mean maximal/minimal ratio was 1.8 +/- 0.08 (range 1.6 to 2.0). The area increased 39 +/- 7.3% (range 16 to 71) with nitroglycerin. In the 10 concentrically shaped lumens (maximal/minimal lumen diameters 1.3 +/- 0.04 [range 1.1 to 1.5]), nitroglycerin increased luminal area by 48 +/- 12.6% (range 0 to 117) (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Artery Disease↗
PubMed1993

Validation by high-frequency epicardial echocardiography of a new method of analyzing coronary angiography quantitatively in coronary artery disease.

In coronary atherosclerosis, the arterial lumen size and shape can be markedly irregular, eccentric and variable. Traditional angiographic interpretation, emphasizing percent diameter stenosis, has been criticized as an inadequate descriptor of such diseased arteries. Computerized quantitative angiographic technologies, yielding a true lumen area measurement, may be superior. High-frequency epicardial echocardiography (HFEE) is a technique that allows on-line evaluation of coronary arterial wall and lumen at the time of cardiac surgery. It has been extensively validated and yields accurate measurements of normal and diseased coronary lumen areas. This study compares quantitative coronary angiography (QCA) estimates of lumen area to those obtained by HFEE to determine if the computerized angiographic method more accurately predicts residual luminal area than traditional angiographic percent diameter stenosis measurements. Although actual luminal morphology was quite variable, there was a good correlation between lumen areas determined by HFEE versus QCA: r = 0.85, n = 67, HFEE = 0.8 QCA - 0.1 (HFEE 4.0 +/- 0.30 mm2, mean +/- SEM range 0.3 to 14.0; QCA 5.1 +/- 0.40 mm2, range 0.7 to 11.8). Percent diameter stenosis determined from the angiograms did not correlate well with HFEE or QCA measurements of residual luminal area. Separation of "normal" arterial segments (defined as < 25% diameter stenosis) from "abnormal" segments (> 50% diameter stenosis) by angiography did not agree with lumen areas as defined by either HFEE or QCA. Better separation occurred when QCA-determined luminal areas were used to separate normal from abnormal arterial segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Variable morphology of coronary atherosclerosis: characterization of atherosclerotic plaque and residual arterial lumen size and shape by epicardial echocardiography.

The purpose of this study was to evaluate the in vivo characteristics of coronary atherosclerosis by using high frequency epicardial echocardiography. High frequency epicardial echocardiography was used to evaluate residual lumen and wall morphology at the sites of maximal coronary atherosclerosis in 26 patients undergoing coronary artery bypass grafting. The maximal/minimal wall thickness ratio was 3.1 +/- 0.2 (mean +/- SEM) with a large range (1.3 to 7.5). Portions of the wall were normal in 16 of 31 lesions; the percent normal circumference ranged from 9% to 85%. Maximal/minimal lumen diameter ratio was 1.5 +/- 0.1 (range 1.1 to 2.9). The shape of the residual coronary lumen was noncircular in 16 lesions: oval in 13 and complex in 3. The residual coronary lumen was eccentrically placed within six arteries. These data emphasize the variability of residual lumen and wall geometry in atherosclerosis.

Coronary Artery Bypass↗
PubMed1992

Coronary microvascular response to exogenously administered and endogenously released acetylcholine.

The objectives of the present study were first, to determine the coronary microvascular response to vagal stimulation and to compare it to exogenously administered acetylcholine, and second, to determine the microvascular response to larger doses of acetylcholine which preferentially increase subendocardial blood flow. In anesthetized cats and dogs, the left ventricular epicardial vasculature was visualized in mid-diastole with stroboscopic epi-illumination. Myocardial perfusion was measured with the radioactive microsphere technique. In cats microvascular diameters were measured at control and following bilateral vagal nerve stimulation (5-30 Hz) or left atrial infusion of acetylcholine (0.4-1.0 micrograms/kg/min). Aortic pressure and heart rate (A-V-sequential pacing) were maintained constant. Vagal stimulation (n = 13) increased myocardial perfusion by 25 +/- 9% (control: 161 +/- 17 ml/min x 100 g). Acetylcholine (n = 13) produced a similar increase in myocardial flow (control: 185 +/- 16 ml/min x 100 g, 30 +/- 9%). Both vagal stimulation and acetylcholine dilated all size arteries and arterioles (51-410 microns; 5 +/- 1% and 11 +/- 2%, respectively). In dogs intracoronary administration of acetylcholine (10 micrograms/min) that increased myocardial flow twofold (control: 129 +/- 7 ml/min x 100 g; 10 micrograms/min: 263 +/- 26 ml/min x 100 g) and increased the endo/epi flow ratio also dilated all vessel sizes. In conclusion, vagal stimulation and exogenously administered acetylcholine produce similar effects on the coronary microcirculation and dilate all size classes of arteries and arterioles in a similar manner. Intracoronary infusion of acetylcholine which preferentially increases subendocardial blood flow also dilates all size classes of microvessels. Thus, the ability of acetylcholine to preferentially increase subendocardial blood flow cannot be explained by a selective dilation of a particular size class of arterioles. These data suggest that neurally released acetylcholine can diffuse to the endothelial layer to release vasodilator substances in vivo.

Acetylcholine↗
PubMed1992

Coronary microvascular response to endothelin is dependent on vessel diameter and route of administration.

Endothelin is a 21-amino acid peptide originally isolated from vascular endothelial cells. In the present study, we examined the effect of topical and intracoronary administration of endothelin-1 on the coronary microcirculation and the effect of inhibition of cyclooxygenase on the microvascular response to intracoronary endothelin. In anesthetized dogs (n = 39), the coronary microcirculation was visualized using stroboscopic epi-illumination synchronized to the cardiac cycle. Topical application of endothelin [(5 x 10(-9) to 10(-8) M] constricted all arteries and arterioles with the degree of constriction inversely related to vessel size. Coronary veins and venules did not constrict to endothelin. Topical application of EDTA (10 mg/ml) reversed the constriction to endothelin in arterioles of all sizes. In contrast, intracoronary administration of endothelin (10(-8) to 10(-7) M) produced dilation of small arterioles (less than 130 microns) and no response of large arterioles (greater than 130 microns). The response of small arterioles to intracoronary endothelin was not altered by inhibition of cyclooxygenase with indomethacin (5 mg/kg); however, large arterioles constricted. Thus the coronary microvascular response to endothelin is dependent on the route of administration. Constriction of arteries and arterioles of all sizes to endothelin is dependent on extracellular calcium. Vasodilator prostaglandins may be released in response to intracoronary administration of endothelin predominantly in larger vessels. Thus the differential response to endothelin with topical and intracoronary administration may reflect a diffusional barrier of the endothelium or release of endothelium-derived relaxing factor and prostaglandins in response to endothelin.

Administration, Topical↗
PubMed1992

Effects of nitroglycerin on the coronary microcirculation in normal and ischemic myocardium.

Nitroglycerin dilates conduit coronary vessels and only transiently increases flow, however the effects of nitroglycerin in the microcirculation of normal myocardium and during myocardial ischemia have not been assessed. The goal of this investigation was to determine the effects of steady-state levels of nitroglycerin on the microcirculation of normal and ischemic myocardium. Microvessels on the left ventricle were viewed using stroboscopic epi-illumination in anesthetized, open-chest dogs. Myocardial perfusion was measured with radioactive microspheres. Aortic pressure and heart rate were kept constant by an aortic snare and left atrial pacing. Microvessel diameters were measured under control conditions and during steady-state infusion of nitroglycerin (n = 11, 0.01-100 micrograms kg-1 min-1, i.v.). Nitroglycerin selectively dilated arteries from 201 to 386 microns, but had no effect on large arterioles less than 200 microns. Total coronary vascular resistance remained constant except at the highest dose. When mean coronary pressure was decreased to 35 mm Hg, small arterioles less than 100 microns dilated. Diameters of larger arterioles decreased. Nitroglycerin (10 micrograms kg-1 min-1, i.v., n = 8) selectively dilated microvessels greater than 200 microns in the region distal to the stenosis, although myocardial perfusion was not affected. Thus, nitroglycerin altered the distribution of microvascular resistance without altering overall resistance. We conclude that steady-state infusion of nitroglycerin selectively dilates coronary arterial microvessels greater than 200 microns. During decreased perfusion pressure, recruitable vasodilation in response to nitroglycerin is due to dilation of microvessels greater than 200 microns.

Animals↗
PubMed1991

Role of medullary lateral reticular formation in baroreflex coronary vasoconstriction.

We have recently identified a polysynaptic pathway traversing discrete regions of the hypothalamus, midbrain, and medulla, along which site-specific electrical and chemical activation produces coronary vasoconstriction as part of a sympathoexcitatory response. We tested for the potential functional significance of this pathway by examining the hypothesis that a medullary component is involved in carotid baroreflex induced coronary vasoconstriction. Coronary flow velocity was measured with a Doppler probe in anesthetized cats. Following vagotomy and propranolol, bilateral carotid occlusion produced an increase in mean arterial pressure (56 +/- 14%, means +/- S.E.M.) and in coronary vascular resistance (51 +/- 13%) which was greater than that (29 +/- 6%) expected from the concurrent rise in arterial pressure during aortic constriction. Bilateral microinjections of lidocaine into the medullary lateral reticular formation attenuated the reflex increase in pressure (11 +/- 2%) and virtually abolished the rise (8 +/- 2%) in coronary resistance. After one hour recovery, carotid occlusion again increased aortic pressure (56 +/- 13%) and coronary vascular resistance (47 +/- 15%). Microinjections of lidocaine outside this medullary region did not impair the coronary vasoconstrictor response to carotid occlusion. We conclude that the medullary lateral reticular formation contains neural elements which participate in baroreflex-induced changes in arterial pressure and coronary vascular resistance. Components of the previously described central coronary vasoconstrictor pathway may play a role in pathophysiological conditions associated with increased coronary vasomotor tone.

Animals↗
PubMed1991

Coronary arterial remodeling studied by high-frequency epicardial echocardiography: an early compensatory mechanism in patients with obstructive coronary atherosclerosis.

Coronary arterial remodeling is a compensatory mechanism that may limit the adverse effects of coronary obstructive lesions by expansion of the entire vascular segment. To determine if this compensatory anatomic change occurs in patients, high-frequency epicardial echocardiography using a 12 MHz transducer was performed during open heart surgery in 33 patients (10 with normal coronary arteries undergoing valvular surgery and 23 with coronary atherosclerosis). From stop-frame videotape high-frequency epicardial echocardiographic images, cross-sectional measurements of luminal area and total arterial area (lumen, intima, media and dense adventitia) were made in the patients with atherosclerosis at the site of arterial lesions and from the most proximal portion of the same artery. Remodeling was defined as enlargement of the total arterial area. In normal arteries measurements were made from proximal and midarterial locations. In the patients with normal coronary arteries, total arterial area, as determined by high-frequency echocardiography, decreased from the proximal site to the midportion of the artery (from 10.4 +/- 0.9 to 8.4 +/- 1.0 mm2, p less than 0.05); luminal area also decreased (from 6.0 +/- 0.6 to 4.5 +/- 0.7 mm2, p less than 0.05). In patients with coronary arterial lesions, luminal area also decreased from the proximal site to the arterial lesion site (from 5.3 +/- 0.6 to 2.3 +/- 0.3 mm2, p less than 0.05), but total arterial area increased (from 11.6 +/- 1.0 to 13.0 +/- 1.0 mm2, p less than 0.05). Of the 25 coronary arteries evaluated, only 4 had angiographic evidence of coronary collateral formation. These data indicate that coronary arterial remodeling is an important compensatory mechanism in obstructive coronary disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Surgical Procedures↗
PubMed1991

Patterns of global and regional systolic and diastolic function in the normal right ventricle assessed by ultrafast computed tomography.

A detailed evaluation of global and regional systolic function and diastolic filling of the human right ventricle has not been previously reported. Ultrafast computed tomography enables simultaneous imaging of the right and left ventricles at an 8 mm slice thickness with a scanning rate of 17 frames/s (50 ms acquisition intervals). In 10 normal men (mean age 26 +/- 4 years) early diastolic filling data were fit to a third order polynomial curve and the peak rate of diastolic filling and time to peak filling were determined globally and regionally at three distinct ventricular levels (apex to base) within each ventricle. The right and left ventricular stroke volumes were not statistically different (89 +/- 8 ml and 90 +/- 8 ml, p = NS), neither were the peak filling rates as referenced to the stroke volume (4.9 +/- 0.9 and 5.3 +/- 0.8 stroke volumes/s, p = NS). Time to peak filling rate was not different between the two ventricles (154 +/- 33 and 161 +/- 18 ms, p = NS). However, reference of stroke volumes and absolute peak filling rates to end-diastolic volumes demonstrated lower dynamic values for the right ventricle (ejection fraction: right ventricle 57 +/- 4%; left ventricle 68 +/- 5%, p less than 0.05, and peak filling rate: right ventricle 2.7 +/- 0.4 end-diastolic volumes/s; left ventricle 3.6 +/- 0.5, p less than 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Effects of coronary artery occlusion in animals with hypertension and left ventricular hypertrophy.

Chronic arterial hypertension (HT) and left ventricular hypertrophy (LVH) increase the morbidity and mortality of acute myocardial infarction in patients. In this article, we discuss earlier studies from Koyanagi et al. in our laboratory that showed that when animals with chronic HT and LVH (HT-LVH) were subjected to acute coronary artery occlusion (CAO), there was a 3.5-fold increase in mortality and a 35% increase in infarct size expressed as a percent of the area at risk. We subsequently determined the effect of HT-LVH on the wavefront of myocardial infarction. Dogs were made hypertensive using a single-kidney, single-clip model of renovascular hypertension that produced mean arterial blood pressure (BP) = 141 +/- 3 mm Hg and left ventricular:body weight = 5.8 +/- 0.1 g/kg (p less than 0.05 vs. control animals). Conscious animals with HT-LVH and control animals were subjected to 1 or 3 h of CAO. Infarct and risk areas were measured using triphenyltetrazolium chloride (TTC) stain and barium angiography, respectively. The results suggested that the wavefront of infarction was accelerated in animals with HT-LVH. Further studies suggested that the wavefront of myocardial infarction could be markedly retarded by normalizing blood pressure (nitroprusside) 1 h following CAO. Recent studies in an animal model of HT-LVH suggested that electrophysiological abnormalities occur when these animals were subjected to CAO. Sixty-five percent of animals with HT-LVH had sudden death during CAO compared to 27% of the control group. We studied whether chronic beta-adrenergic blockade would reduce mortality associated with CAO in animals with HT-LVH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Activation in the region of parabrachial nucleus elicits neurogenically mediated coronary vasoconstriction.

A role for parabrachial nucleus in cardiovascular regulation is suggested by evidence that electrical stimulation in this region elicits increase in heart rate and arterial pressure. We hypothesized that parabrachial nucleus may also be involved in control of coronary vasomotor tone. After beta-adrenergic receptor blockade in anesthetized cats, electrical stimulation in the region of parabrachial nucleus produced no change in heart rate, an increase in arterial pressure (34 +/- 6 mmHg), and a transient reduction in coronary blood flow velocity (-21 +/- 2%). Coronary resistance (72 +/- 9%) and femoral resistance (189 +/- 31%) increased markedly. The decrease in coronary blood flow velocity was abolished by stellate ganglionectomy or alpha 1-adrenergic blockade without altering pressor or femoral responses. Injection of the neurotransmitter L-glutamate or kainic acid into parabrachial nucleus also elicited coronary vasoconstriction. We conclude that electrical or chemical activation in the region of parabrachial nucleus elicits coronary vasoconstriction as part of a generalized sympathetic activation. The fact that the coronary response is elicited by chemical activation suggests that cell bodies in the region of medial parabrachial nucleus and subceruleus, as opposed to fibers of passage, are involved in this central neural coronary vasoconstriction.

Animals↗
PubMed1991

Effect of an arginine analogue on acetylcholine-induced coronary microvascular dilatation in dogs.

The purpose of this study was to elucidate the contribution of endothelium-derived relaxing factor (EDRF) derived from arginine to acetylcholine (ACh)-induced coronary arteriolar vasodilatation in vivo. Experiments were performed in 62 open-chest anesthetized dogs. Internal diameters of small arterioles (less than 120 microns) and large arterioles (greater than 120 microns) were measured using an intravital microscope and stroboscopic epiillumination synchronized to the cardiac cycle. Topically administered NG-monomethyl-L-arginine (L-NMMA, 3 x 10(-4) M) constricted small arterioles (-10.7 +/- 3.1% from control diameter, P less than 0.05), but L-NMMA did not produce vasoconstriction in large arterioles. ACh, in the absence of L-NMMA, caused a dose-dependent vasodilatation in both small and large arterioles. In large arterioles, L-NMMA completely abolished the ACh-induced vasodilatation (10(-5) M topical ACh: from 13.3 +/- 3.0 to -2.0 +/- 1.5%, P less than 0.05; 10(-4) M ACh: from 20.9 +/- 3.9 to -3.0 +/- 1.9%, P less than 0.01). In small arterioles, L-NMMA only partially inhibited the vasodilatation (10(-5) M ACh: from 35.4 +/- 4.0 to 19.0 +/- 2.7%, P less than 0.05; 10(-4) M ACh: from 42.5 +/- 4.8 to 22.6 +/- 3.1%, P less than 0.05). L-Arginine (10(-3) M topically) reversed L-NMMA inhibition of ACh-induced vasodilatation. Persistent dilatation of small arterioles also occurred when NG-nitro-L-arginine rather than L-NMMA was administered.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Coronary vasoconstriction during stimulation in hypothalamic defense region.

Previous studies have identified a site in lateral hypothalamus (LH) in which electrical stimulation elicits coronary vasoconstriction. We injected the retrogradely transported tracer Fast Blue to determine which brain regions project to LH. Projections to or through LH were found from the paraventricular nucleus (PVN) of the hypothalamus, bed nucleus of the stria terminalis (BNST), and dorsal raphe nucleus (DRN). In chloralose-anesthetized cats, electrical stimulation in DRN and BNST failed to increase coronary vascular resistance (CVR). However, stimulation lateral to PVN in the anterior hypothalamic area (AHA), a region not labeled by the tracer, caused a transient decrease in coronary blood flow similar to that elicited from LH. The increase in CVR was accompanied by hemodynamic changes that are characteristic of the defense reaction including a cholinergically mediated decrease in hindquarter vascular resistance. This response is likely due to activation of fibers of passage and not cell bodies, since cell bodies in the region were not retrogradely labeled and coronary vasoconstriction was not seen following microinjection of several excitatory amino acids into AHA. These data suggest that coronary vasoconstriction may be a component of the defense reaction elicited by electrical activation of AHA.

Amidines↗
PubMed1991

Accuracy of exercise electrocardiography in detecting physiologically significant coronary arterial lesions.

The accuracy of exercise electrocardiography in detecting a physiologically significant coronary artery stenosis has been assessed previously by comparing the exercise test with a coronary arteriogram. The inherent inaccuracy of visually determined percent diameter stenosis measurements might have lead to the conclusion that the exercise electrocardiogram was less accurate than it truly was. To determine the accuracy of the exercise electrocardiography in detecting a physiologically significant coronary stenosis, we studied 40 patients with one-vessel, one-lesion coronary artery disease, a normal resting electrocardiogram, and no hypertrophy or prior infarction. Each patient underwent exercise electrocardiography (Bruce protocol) that was interpreted as abnormal if the ST segment developed 0.1-mV or greater depression 80 msec after the J point. The physiological significance of each coronary stenosis was assessed by measuring of coronary flow reserve (peak divided by resting blood flow velocity) in the stenotic artery using a Doppler catheter and intracoronary papaverine (normal, 3.5 or greater peak/resting velocity). The percent diameter and percent area stenosis produced by each lesion were determined using quantitative angiography (Brown/Dodge method). Of the 17 patients with reduced coronary flow reserve (3.5 or greater peak/resting blood flow velocity) in the stenotic artery, 14 had an abnormal exercise electrocardiogram (sensitivity, 0.82; 95% confidence interval, 0.70-0.94). Conversely, 20 of 23 patients with normal coronary flow reserves had normal exercise tests (specificity, 0.87; 95% confidence interval, 0.77-0.97). The exercise electrocardiogram was abnormal in each of 11 patients with markedly reduced coronary flow reserve (less than 2.5 peak/resting velocity) and in three of six patients with moderately reduced reserve (2.5-3.4 peak/resting velocity). The products of systolic blood pressure and heart rate at peak exercise were significantly correlated with coronary reserve in patients with truly abnormal exercise tests. In comparison, the sensitivity (0.61; 95% confidence interval, 0.46-0.76) and specificity (0.73; 95% confidence interval, 0.60-0.86) of exercise electrocardiography in detecting a 60% or greater diameter stenosis may be significantly lower (p less than 0.05). Exercise electrocardiography, therefore, was a good predictor of the physiological significance (assessed by coronary flow reserve) of a coronary stenosis in patients with a normal resting electrocardiogram and no hypertrophy or prior infarction. Its value in a broader and larger patient population will require further study. These results, however, underscore the importance of a physiological gold standard in assessing the accuracy of noninvasive studies for detecting coronary artery disease.

Cardiac Output↗
PubMed1991

Coronary microvascular resistance in hypertensive cats.

Chronic systemic hypertension has been shown to alter the distribution of vascular resistance in many microvascular beds. The purposes of this study were to assess the effects of chronic systemic hypertension on the pressure distribution in the coronary microcirculation and to determine the microvascular site where coronary vascular resistance is increased. Cats were made hypertensive using a one-kidney, one-wrap model (Page model). A servonulling system was used to directly measure pressures in the epimyocardial microvessels of the beating left ventricle in normotensive and hypertensive cats. In chronically hypertensive cats, mean arterial pressure was 153 +/- 5 mm Hg compared with 98 +/- 3 mm Hg in normotensive cats (p less than 0.05). Left ventricular mass was increased approximately 34% in hypertensive cats (9.4 +/- 0.3 versus 7.0 +/- 0.3 g, p less than 0.05). Myocardial perfusion measured using radiolabeled microspheres was not different between hypertensive and normal cats. Coronary vascular resistance of the left ventricle was increased in hypertensive cats (0.90 +/- 0.08 versus 0.66 +/- 0.05 mm Hg x min x 100 g/ml, p less than 0.05). Microvascular pressures were measured in three groups of microvessels: small, less than 200 microns; medium, 200-300 microns; and large, greater than or equal to 300 microns. Mean microvascular pressures of large, medium, and small arterial microvessels in hypertensive cats were 144 +/- 8, 127 +/- 6, and 115 +/- 7 mm Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗