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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cyclical changes in heart rate and systemic blood pressure that accompany apneic events are predominantly mediated by fluctuations in the activity of the autonomic nervous system. Increased vagal efferent parasympathetic activity is responsible for the cyclical reductions in heart rate during apnea. In contrast, the cyclical elevations in systemic blood pressure are believed to result from recurrent peripheral vasoconstriction mediated by repetitive activation of the sympathetic nervous system. Maximal activation and pressures coincide with apnea termination and brief arousal from sleep. These cyclical elevations in systemic pressure during sleep increase ventricular workload and, thereby, may contribute to the development of ventricular hypertrophy. Systemic hypertension is present during wakefulness in approximately 50% of patients with OSA. Although age and obesity are the predominant risk factors for diurnal hypertension, OSA probably makes an independent contribution in younger obese men. Sinus bradycardia, Mobitz type 1 second-degree heart block, and prolonged sinus arrest have all been documented in association with the apneic events. Increased ventricular ectopy has been observed with oxyhemoglobin desaturations below 60%. Myocardial ischemia, infarction, sudden death, and stroke all demonstrate similar circadian variations in time of onset. Peak frequencies occur between 6 AM and noon, generally within several hours of awakening. Although sleep is associated with decreased frequencies of these adverse cardiovascular events in the general population, evidence exists linking REM sleep to an increased risk of myocardial ischemia. In men who habitually snore, epidemiologic data have detected an increased risk for ischemic heart disease and stroke. Habitual snoring has also been associated with an increased risk of sudden death during sleep. In patients with clinically significant OSA, there is reasonable information indicating excessive mortality in the absence of treatment. This mortality is predominantly cardiovascular and tends to occur during sleep.
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PMID:Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. 152 12

The aims of this study were to determine the important prognostic factors at presentation which identify patients with transient ischaemic attacks (TIA) who are at high risk (and low risk) of serious vascular events and to derive a prediction model (equation) for each of the major vascular outcome events. A cohort of 469 TIA patients referred to a University hospital, without prior stroke, were evaluated prospectively and followed up over a mean period of 4.1 years (range 1-10 years). The major outcome events of interest were 1) stroke 2) coronary event and 3) stroke, myocardial infarction or vascular death (whichever occurred first). Prognostic factors and their hazard ratios were identified by means of the Cox proportional hazards multiple regression analysis. The significant adverse prognostic factors (in order of strength of association) for stroke were an increasing number of TIAs in the three months before presentation, increasing age, peripheral vascular disease, left ventricular hypertrophy and TIAs of the brain (compared with the eye); the prognostic factors for coronary event were increasing age, ischaemic heart disease, male sex, and a combination of carotid and vertebrobasilar TIAs at presentation; and for stroke, myocardial infarction or vascular death they were increasing age, peripheral vascular disease, increasing number of TIAs in the three months before presentation, male sex, a combination of carotid and vertebrobasilar TIAs at presentation, TIAs of the brain (compared with the eye), left ventricular hypertrophy and the eye), left ventricular hypertrophy and the eye), left ventricular hypertrophy and the presence of residual neurological signs after the TIA. Prediction models (equations) of both the relative risk and absolute risk of each of the major outcome events were produced, based on the presence or level of the significant prognostic factors and their hazard. Before it can be concluded that our equations accurately predict prognosis and can be generalised to other populations, their predictive power needs to be validated in other, independent samples of TIA patients (which we are currently doing).
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PMID:Transient ischaemic attacks: which patients are at high (and low) risk of serious vascular events? 152 33

In patients with acute myocardial infarction, intravenous nitroglycerin lowers left ventricular filling pressure and systemic vascular resistance. At lower infusion rates (less than 50 micrograms/min) nitroglycerin is principally a venodilator, whereas at higher infusion rates more balanced venous and arterial dilating effects are seen. Patients with left ventricular failure demonstrate increased or maintained stroke volumes, whereas patients without failure show a decrease in stroke volume. All hemodynamic subgroups show a decrease in left ventricular filling pressures and a reduction in electrocardiographic evidence of regional myocardial ischemia. Longer-term infusions (24-48 hours) have been shown to result in myocardial preservation, as assessed by global and regional left ventricular function and laboratory indices of infarct size. Comparison of intravenous nitroglycerin and sodium nitroprusside reveals increased intercoronary collateral flow with nitroglycerin, in contrast to a decrease with nitroprusside, compatible with a "coronary steal." Short-term administration of intravenous nitroglycerin with or without chronic administration of long-acting nitrates have been found both to reduce short-term mortality and to have long-term beneficial effects on left ventricular remodeling in patients with anterior transmural infarctions. Current clinical practice would utilize intravenous nitroglycerin as initial therapy for patients receiving intravenous thrombolytic therapy and/or acute percutaneous transluminal coronary angioplasty within 4-6 hours of the onset of symptoms of acute myocardial infarction, in order to optimize intercoronary collateral flow until reperfusion can be accomplished. Patients reaching the hospital greater than 6 hours but less than 14 hours after symptom onset can still benefit from intravenous nitroglycerin for 24-48 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of nitrates in acute myocardial infarction. 152 29

Hemodynamic changes were studied during two different anesthetic techniques in 54 patients undergoing coronary artery bypass grafting (CABG). All patients had normal to moderately impaired left ventricular function and were randomly assigned to two groups. In 27 patients, high thoracic epidural analgesia (TEA) with bupivacaine 0.375% plus sufentanil 1:200,000 (ie, 5 micrograms/mL) was used in combination with general anesthesia with midazolam/N2O; in the other 27 patients, general anesthesia (GA) with midazolam and sufentanil was used. After induction of epidural analgesia, heart rate and mean arterial pressure (MAP) decreased. Changes in cardiac index, systemic vascular resistance, and pulmonary capillary wedge pressure were not observed, whereas the stroke volume index increased significantly. After induction of intravenous anesthesia MAP decreased (20%) in both groups. During the pre-bypass period, metaraminol was used in 7 of 27 patients in the GA group and in 5 of 27 patients in the TEA group to treat hypotension. Inotopic drugs were used in 5 patients in the GA group and in none in the TEA group to treat a low CO. Ten GA patients and 4 TEA patients developed hypertension after sternal spread and the GA patients required more nitroprusside. Four GA patients developed electrocardiographic evidence of prebypass ischemia and, therefore, more nitroglycerin was needed for treating myocardial ischemia. More sodium nitroprusside was needed in the GA group during cardiopulmonary bypass (CPB) and the post-bypass period to treat hypertension with a high SVR. In conclusion, hemodynamic stability was more pronounced in the TEA than the GA group before and after CPB.
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PMID:Coronary artery bypass grafting using two different anesthetic techniques: Part I: Hemodynamic results. 847 38

Desflurane, a coronary vasodilator, may induce myocardial ischemia in patients with coronary artery disease. To determine whether desflurane is safe to administer to the at-risk patient population (with known coronary artery disease), we compared the incidence and characteristics of perioperative myocardial ischemia in 200 patients undergoing coronary artery bypass graft (CABG) surgery randomly assigned to receive desflurane (thiopental adjuvant) versus sufentanil anesthesia. Under conditions of hemodynamic control, perioperative ischemia was assessed using continuous echocardiography (precordial: during induction; transesophageal: during surgery) and Holter electrocardiography (ECG); hemodynamics (including pulmonary artery pressure) were measured continuously. Hemodynamic results: During induction, no significant changes in hemodynamics occurred in the sufentanil group, while in the desflurane group, heart rate, systemic and pulmonary arterial pressure increased and stroke volume decreased significantly. During the intraoperative period, the incidence of hemodynamic variations was low in both anesthetic groups; however, the prebypass incidence of tachycardia (greater than 120% of preoperative baseline heart rate) was greater in the desflurane group (4 +/- 7% of total time monitored) than in the sufentanil group (1 +/- 6%) (P = 0.0003). Similarly, the incidence of prebypass hypotension (less than 80% of preoperative baseline systolic arterial blood pressure) was greater in the desflurane group (21 +/- 14%) than in the sufentanil group (15 +/- 16%) (P = 0.01). ECG results: Preoperatively, 15% (28/191) of patients developed ECG ischemia, with no difference between patients who received desflurane, 13% (12/96) or sufentanil, 16% (16/95) (P = 0.6). During anesthetic induction, 9% (9/99) of patients who received desflurane developed ECG ischemia, compared with 0% (0/98) who received sufentanil (P = 0.007). During the prebypass period, 5% (10/197) of patients developed ECG ischemia, with no difference between patients who received desflurane, 7% (7/99) or sufentanil, 3% (3/98) (P = 0.3). Postbypass, 12% (24/194) of patients developed ECG ischemic changes, with no difference between patients who received desflurane, 13% (13/97) or sufentanil, 11% (11/96) (P = 0.9). Echocardiographic results: The incidence of precordial echocardiographic ischemia during anesthetic induction was 13% (5/39) in the desflurane group versus 0% (0/29) in the sufentanil group (P = 0.1). Moderate to severe transesophageal echocardiographic (TEE) ischemic episodes occurred in 12% (21/175) of patients during prebypass, with no significant difference between the desflurane group, 16% (15/91) and the sufentanil group, 7% (6/84) (P = 0.09). TEE ischemic episodes occurred in 27% (49/178) of patients during the postbypass period, with no difference between the desflurane, 29% (27/92) and sufentanil, 25% (22/86) groups (P = 0.7).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The risk of myocardial ischemia in patients receiving desflurane versus sufentanil anesthesia for coronary artery bypass graft surgery. The S.P.I. Research Group. 843 40

Abnormalities of left ventricular (LV) systolic performance develop during exercise in patients with coronary artery disease (CAD) as a result of ischemia-induced regional wall motion abnormalities. Like patients with hypertension and those with hypertrophic cardiomyopathy, patients with CAD display abnormalities of LV diastolic performance under basal conditions in the absence of ischemia. The purpose of these studies was to compare the effects of bepridil versus those of propranolol or diltiazem in patients with exertional angina pectoris. LV systolic and diastolic performance were assessed at rest and during peak upright bicycle exercise by first-pass radionuclide ventriculography. Compared with propranolol, bepridil increased exercise capacity, cardiac output, and stroke volume and decreased systemic vascular resistance. Compared with diltiazem, bepridil increased exercise capacity, peak filling rate, and early diastolic filling fraction and decreased systemic vascular resistance, heart rate, time to peak filling rate, and atrial filling volume. Bepridil therapy is associated with improved exercise capacity and decreased anginal frequency and nitroglycerin consumption. In addition, its use is accompanied by favorable changes in LV systolic and diastolic function at rest and during exercise. These changes are consistent with benefits resulting from resolution of myocardial ischemia as well as from positive lusitropic effects of bepridil on the ventricular myocardium.
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PMID:Effects of antianginal therapy on left ventricular systolic and diastolic performance: comparison of the response to bepridil, propranolol, and diltiazem. 155 88

Recent reports of the risk of asymptomatic carotid stenosis have been compromised by flawed patient selection or the performance of a large number of carotid endarterectomies during follow-up. We report the natural history of a randomly selected group of asymptomatic patients (n = 188; 114 males and 74 females) with documented carotid artery disease who were prospectively followed without intervention for up to 8 years. Risk factors included ischaemic heart disease in 17%, diabetes in 10%, hypertension in 46% and 88% were smokers. The degree of internal carotid stenosis was classified by duplex scanning and a total of 259 vessels had evidence of atherosclerosis. Study end-points included TIA, CVA and death. At mean follow-up of 4 years 3% of the 96 patients with internal carotid artery stenosis of less than 50% had died and 2% suffered a stroke. Six per cent of patients with a stenosis of 50-79% had died and 4% and 2% had suffered a CVA and TIA, respectively. In the 59 patients with greater than 80% stenosis 7% had suffered a TIA and an additional 7% a CVA, while 2% had died. None of the patients suffering a stroke had an antecedent TIA. Though the incidence of ischaemic events is significantly higher in patients with greater than 80% stenosis the incidence of unheralded stroke remains low. We therefore continue to recommend a conservative approach to the management of asymptomatic carotid stenosis.
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PMID:Asymptomatic carotid stenosis: a benign lesion? 155 61

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.
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PMID:Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency. 157 47

Mortality from cardiovascular disease (CVD) for the period 1979 to 1985 in the Atlanta metropolitan population was reviewed for racial differences. About 28% of the population was black in 1980. Of 22,585 deaths from hypertension, stroke, ischemic heart disease, and atherosclerosis, 78.7% occurred among whites and 21.3% among blacks. Overall, ischemic heart disease accounted for 47.7% of these four types of CVD deaths for both races and sexes. Age-specific and age-adjusted rates were compared. Among these four causes of death, blacks have the greatest excess of deaths from hypertension over whites for both males and females; the excesses were more than 200% when the rates were age-adjusted. The excess risk of death from hypertension occurred for all ages in blacks, with an excess of about 10 times in 30- to 49-year-olds. An excess risk from stroke also occurred in blacks below the age of 75; the risk reversed afterward. The age-specific mortality rates revealed an excess from ischemic heart disease only between the ages of 30 and 59 years and from atherosclerosis between 40 and 59 years of age for black men. This age-related crossover in females did not occur until the age of 75 years for deaths attributed to these causes. These data suggest that blacks were at highest risk for all four causes at younger age groups.
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PMID:Racial differences in mortality from cardiovascular disease in Atlanta, 1979-1985. 157 1

Three social network measures were obtained from a randomly sampled cohort of 2603 HMO members in 1970-71. Mortality and first incidence of ischemic heart disease, cancer, stroke, and hypertension were assessed over the next 15 years. Outcome data were adjusted for age, sex, smoking, SES, and baseline health status. Persons with histories of a given morbidity at or prior to baseline were excluded from the analyses of that morbidity. Social network measures, particularly network scope (a measure of the number of different domains in which a person has social contacts), were powerful predictors of 15-year mortality hazard, but weak predictors of incident disease. Only network scope predicted IHD incidence, and none of the other morbidities was predicted by the social network measures. However, social network measures were strong predictors of both cause-specific and all-cause mortality among persons who had incident cases of IHD, cancer, and stroke. These data suggest that social networks may be more effective in supporting recovery after illness has occurred than in preventing the incidence of new disease.
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PMID:Social networks as predictors of ischemic heart disease, cancer, stroke and hypertension: incidence, survival and mortality. 160 5


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