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Biomedical subjects

S E Epstein

Publications and source records attributed to S E Epstein.

At least 145 records · Page 8Linked to original sources
PubMed1987

Dynamic limitation of coronary vasodilator reserve in patients with dilated cardiomyopathy and chest pain.

Twenty-six patients with dilated cardiomyopathy and angiographically normal coronary arteries, 12 of whom gave a history of anginal chest pain, underwent noninvasive and invasive hemodynamic study. During treadmill exercise testing, patients with a history of angina demonstrated worse effort tolerance (7.4 +/- 4.9 versus 13.6 +/- 5.1 minutes, p less than 0.005) and a lower end-exercise systolic blood pressure-heart rate product (17.9 +/- 3.4 versus 23.6 +/- 4.9 mm Hg.beats/min x 10(3), p less than 0.005) compared with patients without a history of angina. During rapid atrial pacing after ergonovine, 0.15 mg intravenously, 11 of the 12 patients with a history of angina experienced their typical chest pain, in contrast to only 1 of 12 patients without a history of angina. The angina group, compared with the nonangina group, had significantly lower great cardiac vein flow (118 +/- 24 versus 160 +/- 43 ml/min, p less than 0.01), and higher coronary resistance (0.87 +/- 0.21 versus 0.66 +/- 0.25 mm Hg.min/ml, p less than 0.05), significant widening of the arterial--great cardiac vein oxygen difference and a significant fall in cardiac index during pacing. Further, ergonovine resulted in higher coronary resistance during pacing in the angina group compared with pacing alone (+0.16 +/- 0.16 mm Hg min/ml, p less than 0.01), in the absence of significant reduction in epicardial coronary artery luminal diameter. After dipyridamole, 0.5 to 0.75 mg/kg intravenously, to 21 patients, the 7 patients with a history of angina had significantly lower flow (149 +/- 37 versus 218 +/- 73 ml/min, p less than 0.05) and higher coronary resistance (0.59 +/- 0.09 versus 0.43 +/- 0.17 mm Hg.min/ml, p less than 0.05) than did the nonangina group. It is concluded that patients with dilated cardiomyopathy and chest pain unrelated to epicardial coronary artery disease exhibit impaired vasodilator responses to both metabolic and pharmacologic stimuli, and an increased sensitivity to the vasoconstrictor effects of ergonovine. Whether these findings are of etiologic or long-term prognostic significance is unknown.

Adult↗
PubMed1987

Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy.

Fifty patients with hypertrophic cardiomyopathy underwent invasive study of coronary and myocardial hemodynamics in the basal state and during the stress of pacing. The 23 patients with basal obstruction (average left ventricular outflow gradient, 77 +/- 33 mm Hg; left ventricular systolic pressure, 196 +/- 33 mm Hg, mean +/- 1 SD) had significantly lower coronary resistance (0.85 +/- 0.18 versus 1.32 +/- 0.44 mm Hg X min/ml, p less than 0.001) and higher basal coronary flow (106 +/- 20 versus 80 +/- 25 ml/min, p less than 0.001) in the anterior left ventricle, associated with higher regional myocardial oxygen consumption (12.4 +/- 3.6 versus 8.9 +/- 3.3 ml oxygen/min, p less than 0.001) compared with the 27 patients without obstruction (mean left ventricular systolic pressure 134 +/- 18 mm Hg, p less than 0.001). Myocardial oxygen consumption and coronary blood flow were also significantly higher at paced heart rates of 100 and 130 beats/min (the anginal threshold for 41 of the 50 patients) in patients with obstruction compared with those without. In patients with obstruction, transmural coronary flow reserve was exhausted at a heart rate of 130 beats/min; higher heart rates resulted in more severe metabolic evidence of ischemia with all patients experiencing chest pain, associated with an actual increase in coronary resistance. Patients without obstruction also demonstrated evidence of ischemia at heart rates of 130 and 150 beats/min, with 25 of 27 patients experiencing chest pain. In this group, myocardial ischemia occurred at significantly lower coronary flow, higher coronary resistance and lower myocardial oxygen consumption, suggesting more severely impaired flow delivery in this group compared with those with obstruction. Abnormalities in myocardial oxygen extraction and marked elevation in filling pressures during stress were noted in both groups. Thus, obstruction to left ventricular outflow is associated with high left ventricular systolic pressure and oxygen consumption and therefore has important pathogenetic importance to the precipitation of ischemia in patients with hypertrophic cardiomyopathy. Patients without obstruction may have greater impairment in coronary flow delivery during stress.

Adult↗
PubMed1987

Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction.

Patients with anginal chest pain despite angiographically normal coronary arteries and left ventricles may have abnormalities of coronary flow reserve. Twenty-five patients were found to have limited flow reserve during rapid atrial pacing after administration of 0.15 to 0.30 mg iv ergonovine, associated with precipitation of chest pain and hemodynamic and metabolic evidence of myocardial ischemia. No significant narrowing occurred in epicardial coronary artery luminal diameter. An additional 15 patients had no chest pain during pacing; because they developed significantly higher great cardiac vein flow and lower coronary resistance they were considered to have normal vasodilator reserve. After administration of dipyridamole (0.5 to 0.75 mg/kg iv), the lowest absolute levels to which coronary resistance fell (0.79 +/- 0.23 vs 0.47 +/- 0.12 mm Hg X min/ml; p less than .001) and the maximal absolute levels to which great cardiac vein flow rose (134 +/- 34 vs 202 +/- 45 ml/min; p less than .001) were impaired in the 25 patients with ergonovine-induced flow limitation compared with the 15 patients without flow limitation after ergonovine. In addition, 18 of the 25 patients with limited flow reserve after dipyridamole experienced chest pain despite an increase in coronary flow. In these patients, dipyridamole-induced increased flow across small prearteriolar coronary arteries, which were narrowed because of abnormal tonus or sensitivity to vasoconstrictor stimuli, could have resulted in a transmural redistribution of blood flow away from the subendocardium, precipitating subendocardial ischemia. These studies suggest that patients with anginal chest pain despite normal epicardial coronary arteries may have exaggerated coronary responses to vasoconstrictor stimuli, which can result in myocardial ischemia during stress, as well as attenuated responses to coronary vasodilator stimuli.

Adult↗
PubMed1987

Myocardial perfusion abnormalities in patients with hypertrophic cardiomyopathy: assessment with thallium-201 emission computed tomography.

Myocardial ischemia may play a critical role in the symptomatic presentation and natural history of hypertrophic cardiomyopathy (HCM). To assess the relative prevalence and functional significance of myocardial perfusion abnormalities in patients comprising the broad clinical spectrum of HCM, we studied 72 patients (ages 12 to 69 years, mean 40) using thallium-201 emission computed tomography. Imaging was performed immediately after maximal exercise and again after a 3 hr delay. Regional perfusion defects were identified in 41 of the 72 patients (57%). Fixed or only partially reversible defects were evident in 17 patients, 14 of whom (82%) had left ventricular ejection fractions of less than 50% at rest. Twenty-four patients demonstrated perfusion defects during exercise that completely reversed at rest; all had normal or hyperdynamic left ventricular systolic function (ejection fraction greater than or equal to 50%). Perfusion abnormalities were present in all regions of the left ventricle. However, the fixed defects were observed predominantly in segments of the left ventricular wall that were of normal or only mildly increased (15 to 20 mm) thickness; in contrast, a substantial proportion (41%) of the completely reversible defects occurred in areas of moderate-to-marked wall thickness (greater than or equal to 20 mm, p less than .001). Neither a history of chest pain nor its provocation with treadmill exercise was predictive of an abnormal thallium study, since regional perfusion defects were present in 10 of 18 (56%) completely asymptomatic patients, compared with 31 of 54 (58%) symptomatic patients. These data indicate that myocardial perfusion abnormalities occur commonly among patients with HCM. Fixed or only partially reversible defects suggestive of myocardial scar and/or severe ischemia occur primarily in patients with impaired systolic performance. Completely reversible perfusion abnormalities occur predominantly in patients with normal or supranormal left ventricular systolic function. Such dynamic changes in regional thallium activity may reflect an ischemic process that contributes importantly to the clinical manifestations and natural history of HCM.

Adolescent↗
PubMed1987

Dynamic obstruction to left ventricular outflow: the case for its existence in hypertrophic cardiomyopathy.

The debate and controversy over the hemodynamics of obstruction and left ventricular ejection in HCM is an interesting and complex one in which periodic disagreement has appeared during the last 20 years. We believe that the available data unequivocally support the concept that in those patients with HCM who have left ventricular outflow gradients measured at catheterization (and who have associated marked SAM) a mechanical impediment to forward flow, and thus true obstruction to left ventricular outflow, does exist. Most importantly, the gradient has critical clinical implications by virtue of the markedly elevated intraventricular systolic pressures associated with it. These chronically elevated pressures are potentially detrimental to the left ventricle (a view held even by investigators opposed to the term "obstruction"), by virtue of increasing systolic myocardial wall stress and myocardial oxygen demand. Therefore, surgical abolition of the obstruction and normalization of these pressures remains an important and rational therapeutic objective in those severely symptomatic patients who have obstruction to left ventricular outflow and who have failed to benefit from drug therapy.

Cardiomyopathy, Hypertrophic↗
PubMed1987

Morphologic evidence for "small vessel disease" in patients with hypertrophic cardiomyopathy.

Many patients with hypertrophic cardiomyopathy (HCM) have signs and symptoms or metabolic and hemodynamic evidence of myocardial ischemia and dysfunction in the absence of extramural coronary atherosclerosis. To investigate the possibility that a form of "small vessel disease" could account for these findings, a histologic analysis of left ventricular myocardium obtained at necropsy was carried out in 48 patients with hypertophic cardiomyopathy and in 68 controls with either normal hearts or acquired heart disease. In HCM, abnormal intramural coronary arteries (IMCA) were characterized by thickening of the vessel wall and an apparent decrease in luminal size (external arterial diameter less than 1500 micron; average 300 micron). The wall thickening was due to proliferation of medial and/or intimal components, particularly smooth muscle cells and collagen. Of the 48 patients with HCM,40 (83%) had abnormal IMCAs located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (nine patients); an average of 3.0 +/- 0.7 IMCA were identified per tissue section. Altered IMCAs were also significantly more common in tissue sections having considerable myocardial fibrosis (31 out of 42, 74%) than in those with no or mild fibrosis (31 or 102, 30%; p less than 0.001). Abnormal IMCA wera also identified in 3 out of 8 infants who died of HCM before 1 year of age. In contrast, only rare altered IMCA were identified in six (9%) of the 69 control patients, and those arteries showed only mild thickening of the wall and minimal luminal narrowing (abnormal IMCA per section: 0.1 +/- 0.05: p less than 0.001). Moreover, of those patients who did show abnormal IMCA, such vessels were about twenty times more frequent in patients with HCM (0.9 +/- 0.2/cm2 myocardium) than in controls (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal IMCA with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with HCM at necropsy, and may represent a congenital component of the underlying cardiomyopathic process. Although the clinical significance of "small vessel coronary artery disease" in HCM is unclear, the occurrence of structurally altered IMCA within or adjacent to areas of substantial myocardial fibrosis suggests a causal role for these arteries in producing ischemia.

Adult↗
PubMed1986

Severe functional limitation in patients with hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy.

Ten patients with nonobstructive hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy who had severe symptoms of cardiac failure are described. During a mean follow-up period of 7 years, 6 of these 10 patients showed a substantial increase in left ventricular internal dimension (6 to 15 mm, mean 10) as assessed with M-mode echocardiography, although absolute left ventricular cavity size remained within normal limits in 5 of the 6. Four patients demonstrated substantial septal thinning (5 to 14 mm, mean 8). Left ventricular diastolic function, assessed by radionuclide angiography in nine patients, was impaired in eight who showed decreased peak filling rate (less than 2.5 end-diastolic volumes/s) and prolonged time to peak rate of filling (greater than or equal to 180 ms). Furthermore, left ventricular systolic function, usually supernormal in patients with hypertrophic cardiomyopathy, was depressed (ejection fraction less than or equal to 45%) in six patients. Hence, a subset of patients was identified with nonobstructive hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy who experienced severe cardiac symptoms. The majority of these patients showed both systolic and diastolic left ventricular dysfunction in the presence of a progressive increase in left ventricular internal dimension (but without absolute left ventricular dilation) or ventricular septal thinning or both. Such patients may represent an important component of the natural history of hypertrophic cardiomyopathy which has not been previously fully appreciated.

Adolescent↗
PubMed1986

Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy.

Many patients with hypertrophic cardiomyopathy have signs and symptoms of myocardial ischemia and dysfunction. Although hypertrophy and increased left ventricular pressure can account for such abnormalities, altered small intramural coronary arteries have also been described in such patients. To determine the prevalence and extent as well as the clinical relevance of abnormal intramural coronary arteries, a histologic analysis of left ventricular myocardium obtained at necropsy was performed in 48 patients with hypertrophic cardiomyopathy (but without atherosclerosis of the extramural coronary arteries) and in 68 control patients with either a normal heart or acquired heart disease. In hypertrophic cardiomyopathy, abnormal intramural coronary arteries were characterized by thickening of the vessel wall and a decrease in luminal size. The wall thickening was due to proliferation of medial or intimal components, or both, particularly smooth muscle cells and collagen. Of the 48 patients with hypertrophic cardiomyopathy, 40 (83%) had abnormalities of intramural coronary arteries located in the ventricular septum (33 patients), anterior left ventricular free wall (20 patients) or posterior free wall (9 patients); an average of 3.0 +/- 0.7 abnormal arteries were identified per tissue section. Altered intramural coronary arteries were also significantly more common in tissue sections having considerable myocardial fibrosis (31 [74%] of 42) than in those with no or mild fibrosis (31 [30%] of 102; p less than 0.001). Abnormal intramural coronary arteries were also identified in three of eight infants who died of hypertrophic cardiomyopathy before 1 year of age. In contrast, only rare altered intramural coronary arteries were identified in 6 (9%) of the 68 control patients (0.1 +/- 0.05 abnormal arteries per section; p less than 0.001) and those arteries showed only mild thickening of the wall and minimal luminal narrowing. Moreover, of those patients with abnormal intramural coronary arteries, such vessels were about 20 times more frequent in patients with hypertrophic cardiomyopathy (0.9 +/- 0.2/cm2 myocardium) than in control patients (0.04 +/- 0.02/cm2 myocardium). Hence, abnormal intramural coronary arteries with markedly thickened walls and narrowed lumens are present in increased numbers in most patients with hypertrophic cardiomyopathy studied at necropsy and may represent a congenital component of the underlying cardiomyopathic process.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1986

Causes of sudden death in competitive athletes.

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.

Adolescent↗
PubMed1986

Sudden death and the competitive athlete: perspectives on preparticipation screening studies.

Sudden death in healthy athletes is uncommon but, when it occurs, the primary mechanism is cardiovascular. The major cause of sudden death in the young athlete is hypertrophic cardiomyopathy or related conditions characterized by left ventricular hypertrophy, aortic rupture due to cystic medial necrosis and congenital coronary artery abnormalities. In the middle-aged or older athlete, coronary artery disease is the most significant cause of sudden death. Noninvasive screening procedures are currently available that can detect most subjects at risk of sudden death. However, although some potentially lethal diseases can be excluded by a relatively simple screening program, other diseases require expensive procedures, such as echocardiography and exercise electrocardiographic stress testing. This means that the sensitivity of detecting diseases leading to sudden death increases in proportion to the financial resources that can be applied to the screening program. Thus, when a screening program designed to identify all cardiac diseases that have the potential to cause sudden death is planned by a community, school or nonprofessional athletic team, the costs will almost undoubtedly be considered prohibitive. The practicality of applying a community- or school-initiated screening program can be questioned because of the very low incidence of sudden unexpected death in young healthy individuals. It is therefore likely that comprehensive screening programs will be confined to individuals or organizations with adequate financial resources. Less expensive, limited screening can be undertaken by individuals or groups to identify some subjects at risk of sudden death during athletic competition.

Adult↗
PubMed1985

Hemodynamic principles in the control of coronary blood flow.

The effects of atherosclerotic epicardial stenoses on coronary vascular resistance can be understood in terms of basic principles of fluid mechanics. Resistance is directly related to the pressure drop across the stenosis and inversely related to flow. Even with a fixed anatomic stenosis, however, resistance is not fixed; it increases as flow across the stenosis increases. This exacerbates the pressure drop across the stenosis that develops as a result of flow; at high flows, large pressure drops can occur. This characteristic of flow through stenotic lesions can contribute to a "steal" phenomenon between either epicardial or intramural coronary arteries. Studies have also shown the clinical importance and influence of dynamic alterations in coronary resistance, occurring either at the large or small vessel level. In addition, compressive forces exerted by the myocardium or by elevated intraventricular pressures can increase coronary vascular resistance, and thus interfere with myocardial perfusion. All of these factors must be considered in order to obtain a comprehensive understanding of the mechanisms leading to myocardial ischemia and, therefore, to the clinical syndrome of angina pectoris.

Angina Pectoris↗
PubMed1985

Efficacy of calcium channel blocker therapy for angina pectoris resulting from small-vessel coronary artery disease and abnormal vasodilator reserve.

Abnormal vasodilator reserve of the coronary microcirculation is a frequent mechanism of angina pectoris in patients with angiographically normal coronary arteries. To assess the effect of calcium channel blocking agents on symptoms and exercise capacity, 26 patients shown to have angina pectoris because of abnormally small coronary arteries and limited vasodilator reserve underwent randomized, double-blind, placebo-controlled outpatient study, with 1 month for each period. An unblinded lead-in phase determined the best dose of verapamil (17 patients) or nifedipine (9 patients). Exercise testing using bicycle ergometry was performed at the end of each period. Four patients interrupted the placebo period and 1 patient interrupted both placebo and drug period because of frequent and severe chest pain. While receiving calcium channel blocker drugs, patients who completed both phases of the study recorded fewer episodes of angina (21 +/- 21 vs 35 +/- 27, p less than 0.001) and consumed fewer nitroglycerin tablets (23 +/- 27 vs 41 +/- 50, p less than 0.001) than during the placebo period. Exercise duration was slightly but significantly prolonged (278 +/- 129 vs 231 +/- 136 seconds, p less than 0.025) during drug treatment compared with placebo, and significantly fewer patients terminated exercise with chest pain while receiving drug treatment. Subjectively, 22 of 26 patients felt better on the calcium channel blocker than on placebo. Thus, calcium channel blocker therapy appears to be beneficial in controlling angina and improving exercise tolerance in patients with angina pectoris resulting from abnormally small coronary arteries and limited vasodilator reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Comparative effects of calcium-channel blocking agents on left ventricular function during acute ischemia in dogs with and without congestive heart failure.

To examine the relative potencies of verapamil, nifedipine and diltiazem on left ventricular (LV) function under ischemic conditions, 20 conscious closed-chest dogs that had partial occlusion of their circumflex coronary arteries were studied. Myocardial blood flow was measured by microspheres, LV function by radionuclide angiography. Drug effects were compared at doses causing equal decreases in mean arterial pressure (MAP) and in coronary vascular resistance of the nonischemic zone. Global ejection fraction (EF) and EF of the ischemic region were significantly decreased by verapamil (p less than 0.002) and increased by nifedipine (p less than 0.001); diltiazem caused no significant changes. Verapamil significantly increased peak diastolic filling rate (p less than 0.001); nifedipine also increased diastolic filling rate but only at doses that markedly decreased MAP and coronary vascular resistance. Diltiazem was not significantly different from placebo. For doses causing an equal decrease in MAP, verapamil decreased heart rate (p less than 0.001), and diltiazem and nifedipine increased heart rate (p less than 0.05). Myocardial ischemic zone flow remained unchanged during placebo, verapamil, diltiazem or nifedipine infusion. To study the influence of heart failure on the hemodynamic effects of the calcium-channel blocking agents, 6 foxhounds underwent total occlusions of the left anterior descending coronary artery, resulting in myocardial infarction, volume loading to increase left atrial pressure and partial occlusion of the circumflex coronary artery. Verapamil depressed global left ventricular ejection fraction and increased left atrial pressure to as high as 40 to 45 mm Hg. In contrast, nifedipine decreased left atrial pressure and increased global EF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Chest pain and "normal" coronary arteries--role of small coronary arteries.

To study the mechanism of chest pain in patients with insignificant epicardial coronary artery disease, 50 patients underwent great cardiac vein (GCV) flow, oxygen content and lactate determinations at rest and during pacing, and left ventricular end-diastolic pressure (LVEDP) measurements at rest and after pacing. Twenty-four patients having typical chest discomfort during pacing demonstrated significantly lower increase in flow from baseline (36 +/- 18% versus 86 +/- 24%, p less than 0.001) and decrease in coronary resistance (-17 +/- 12% versus -43 +/- 7%, p less than 0.001) compared with 26 patients without pacing-induced chest pain, despite no significant difference in myocardial oxygen consumption (MVO2) between the 2 groups. Lactate consumption at a heart rate (HR) of 150 beats/min was significantly less (28.3 +/- 21.5 versus 51.3 +/- 35.8 mM X ml/min, p less than 0.001) and the increase in LVEDP from rest to after pacing was significantly greater (5 +/- 2 versus 1 +/- 2 mm Hg, p less than 0.001) in the chest pain group. After administration of ergonovine, 0.15 mg intravenously, to 46 of these patients, 31 had typical pain either at rest (1 patient) or during pacing. This group had significantly lower increase in flow (38 +/- 20% versus 107 +/- 38%, p less than 0.001), and decrease in coronary resistance (-16 +/- 12% versus -45 +/- 11%, p less than 0.001) compared with the 15 patients not having chest pain, despite no significant difference in MVO2 between the 2 groups. Patients with chest pain also had lower lactate consumption at a HR of 150 beats/min (39.2 +/- 23.6 versus 65.3 +/- 46.3 mM X ml/min, p less than 0.01), greater arterial-GCV oxygen difference (12.5 +/- 1.3 versus 11.6 +/- 1.0 ml O2/100 ml, p less than 0.05), and a more marked increase in LVEDP from rest to after pacing (11 +/- 3 versus 5 +/- 2 mm Hg, p less than 0.001). Quantitative coronary arteriography demonstrated no significant luminal narrowing of the epicardial coronary arteries in response to ergonovine. These data are consistent with the hypothesis that some patients with chest pain and angiographically normal epicardial coronary arteries have dynamic abnormalities of the small coronary arteries or coronary microcirculation that cause abnormal vasodilator reserve or vasoconstriction, resulting in myocardial ischemia and angina pectoris.

Adult↗
PubMed1985

Dynamic coronary obstruction as a cause of angina pectoris: implications regarding therapy.

The strong link demonstrated at autopsy between coronary atherosclerosis and angina pectoris led to the important concept that a fixed obstruction of 1 or more coronary arteries was the pathophysiologic cause of angina: myocardial ischemia and angina occurred when myocardial oxygen demand out-stripped the capacity of the diseased coronary artery to deliver oxygen. Therapeutic strategies were based on attempts to lower myocardial oxygen needs induced by physical and emotional stress. However, the finding that dynamic increases in coronary vascular resistance can also either precipitate ischemia or reduce the threshold of myocardial oxygen consumption (MVO2) at which it occurs has profoundly altered our understanding of the pathophysiologic features of angina and, therefore, its treatment. Dynamic coronary obstruction can occur at the large-vessel level, causing Prinzmetal's or variant angina. It is also possible that in some patients a continuum of large-vessel coronary vasoconstrictor tone exists, causing the common clinical situation manifested by angina with variable thresholds of onset. Recent studies have demonstrated that increases in the resistance offered to flow by small coronary arteries too small to be imaged by angiography can also decrease anginal threshold. The fact that ischemia can be precipitated by dynamic increases in large- or small-vessel coronary resistance has important implications for the therapy of angina pectoris. In those persons who mostly have a dynamic component contributing to their coronary obstruction, primary intervention with vasodilator therapy, including nitrates and calcium-channel blocking agents, are probably most effective therapeutically.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗