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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic effects of acebutolol, a cardioselective beta-adrenergic blocker, and of propranolol, a nonselective beta blocker, were evaluated. Our subjects were 20 men with chronic stable angina; none had diabetes. An initial 4-wk, single-blind control phase was followed by two drug treatment periods, each a 3-wk double-blind titration phase (using increasing doses of acebutolol or propranolol), followed by a 5-wk double-blind maintenance phase. Metabolic studies were performed at the end of the control and maintenance phases. Propranolol induced elevation in basal serum glucose concentrations and both propranolol and acebutolol decreased glucose tolerance at 2.5 and 3 hr. There was no noticeable effect on insulin secretion by either drug. Neither propranolol nor acebutolol induced hyperlipidemia. There was a small decrease in total serum cholesterol after propranolol. Both drugs decreased low-density lipoprotein cholesterol. No effects were noted on the levels of serum triglycerides, high-density lipoprotein cholesterol, or free fatty acids.
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PMID:Glucose and lipid metabolism during acebutolol and propranolol therapy of angina in nondiabetic patients. 633 62

Coronary atherosclerosis is the process underlying virtually all the clinical manifestations of ischemic heart disease. When ulcer or fissure in the fibrous cap of the atheroma occur, platelet adhesion to subendothelium, aggregation and further platelet recruitment culminate in thrombus formation. These mechanisms are known to be responsible for most cases of acute events in patients with ischemic heart disease. Inside platelets, aspirin blocks the synthesis of thromboxane A2 by irreversibly inhibiting cyclooxygenase. Aspirin is recommended not only for treatment of patients with acute coronary syndromes (unstable angina, acute myocardial infarction), but also for secondary prevention of vascular events in chronic coronary syndromes. Aspirin prevents myocardial infarction in patients with chronic stable angina and reduces mortality, reinfarction and stroke in survivors of an acute myocardial infarction. Aspirin, alone or in combination with dipyridamole, prevents early and late occlusion of aortocoronary vein grafts. It is useful also in patients undergoing coronary angioplasty. Such benefits extend to all patients regardless of age, sex, history of hypertension or diabetes. Higher daily doses (900-1500 mg) are not more effective than lower doses (75-325 mg). Other antiplatelet drugs are not more effective than aspirin, which has the best risk-to-benefit and cost-to-benefit ratios. Ticlopidine is a reasonable alternative for use in preventing vascular events among patients intolerant to aspirin. Warfarin is an effective antithrombotic alternative to aspirin for secondary prevention after a myocardial infarction. However aspirin is easier to administer and follow-up when compared with warfarin. Warfarin should be preferred in high risk patients with left ventricular dysfunction with or without a mural thrombus, and those with associated atrial fibrillation.
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PMID:[Low-dose aspirin in the long-term treatment of the patient with ischemic heart disease]. 763 59

The prognosis during 1 year of follow-up in 715 patients admitted to one single hospital due to suspected acute myocardial infarction (AMI) with a history of unstable angina pectoris immediately preceding hospitalization is described. AMI developed in 192 patients (27%) during the first three days and in 255 patients (38%) during the first year. The mortality during hospitalization was 7% (50 patients) and during 1 year 19% (130 patients). Of the nonsurvivors, 54% died of AMI, 28% of congestive heart failure, and 20% of cardiogenic shock. Based on simple clinical parameters on admission to the emergency room, risk indicators for death during the following year could be identified as follows, in the order of significance: high age (p < 0.001), ST-segment depression on admission (p < 0.001), and a history of diabetes mellitus (p < 0.05). At admission to the emergency room, risk indicators for development of AMI during the following year were as follows: initial degree of suspicion of AMI (p < 0.001), electrocardiographic signs of acute ischemia on admission (p < 0.001), ST-segment elevation on admission (p < 0.01), age (p < 0.05), and lack of a previous history of chronic stable angina pectoris (p < 0.05). We conclude that, among patients admitted to hospital due to suspected AMI with a history of unstable angina pectoris immediately preceding hospitalization, 38% developed a confirmed infarction and 19% died during the following year.
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PMID:One-year prognosis in patients hospitalized with a history of unstable angina pectoris. 850 73

In patients who present with unheralded myocardial infarction both the severity and the extent of coronary atherosclerosis appear to be less than that in patients with chronic stable angina, thus suggesting that, in the latter, protective factors may prevent or delay the evolution towards acute coronary syndromes. Therefore, risk factors were compared in 88 consecutive patients (73 men; mean age 56 +/- 9 years) with unheralded myocardial infarction and a single, discrete, > 70% stenosis in the proximal right, left circumflex or left anterior descending coronary artery (Group 1) and in 55 consecutive patients (46 men; mean age 58 +/- 9 years with chronic stable angina and multiple, diffuse, > 70% stenoses localized both in the right and left coronary arteries (Group 2). Continuous data are presented as mean value +/- 1 SD, proportions as percentages. In Group 1 mean serum levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides were similar to those in mg/dl, p = 0.93 and 160 +/- 87 vs 155 +/- 76, p = 0.74, respectively) while the mean serum level of high-density lipoprotein cholesterol was higher in Group 2 (49 +/- 4 vs 46 +/- 4 mg/dl, p = 0.005). The prevalence of a positive family history of ischemic heart disease, hypertension and smoking habit were similar in the two groups, while the prevalence of diabetes mellitus was higher in Group 2 (29 vs 6%, p = 0.001). Thus, in patients with otherwise similar coronary risk factors, higher levels of high-density lipoprotein cholesterol and diabetes mellitus appear to be associated with a reduced tendency of coronary atherosclerosis to cause acute coronary syndromes.
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PMID:Risk factors in patients with different clinical and angiographic manifestations of ischemic heart disease. 854 20

This investigation examines whether serum lipoprotein levels in patients with diabetes mellitus and in those with coronary artery disease are associated with lower heart rate variability (HRV). The study group consisted of 58 subjects divided into 3 groups: normal subjects, chronic stable angina, and type 1 diabetes. Twenty-four-hour ambulatory electrocardiographic recordings were analyzed in the time and frequency domains; standard instantaneous autonomic testing was also performed. On 24-hour ambulatory recordings, patients with chronic stable angina had significantly lower HRV than normals, and diabetics had a more marked reduction in HRV than both normals and anginal patients. When anginal patients and diabetics were stratified by total serum and low-density lipoprotein (LDL) cholesterol levels, diabetics with elevated total and LDL cholesterol had an additional, significant decrease in HRV parameters. No such difference was demonstrated in patients with stable angina. No significant correlations were noted for high-density lipoprotein (HDL) cholesterol, triglycerides, or total cholesterol/HDL ratio and HRV in diabetics or patient with angina. Diabetics with markedly abnormal peripheral reflexes had significantly higher triglycerides and total cholesterol/HDL ratios. Finally, standard tests of autonomic function did not correlate with total, LDL, HDL cholesterol levels, total cholesterol/HDL ratio, or triglycerides. Thus, we found a relation between atherogenic lipid levels and reduced HRV in diabetic patients that has not been previously identified.
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PMID:Relation of heart rate variability and serum lipoproteins in type 1 diabetes mellitus and chronic stable angina pectoris. 957 51

The purpose of our investigation was to compare circadian patterns of heart rate variability as assessed by 24-h ambulatory electrocardiographic (ECG) recordings in normal subjects, chronic stable angina, and Type 1 diabetes mellitus. The study population consisted of three groups: 12 normal subjects, 23 chronic angina patients, and 23 Type 1 diabetics. For purposes of analyzing circadian variation, the ECG recordings were divided into daytime (08:00-00.00 h) and night-time (00:00-08:00 h) periods. Analysis was performed for all time and frequency domain measures of heart rate variability, attempting to identify differences in day-to-night variability among these three groups. All time domain parameters except standard deviation of all 5-min mean RR intervals, and all frequency domain indices maintain significant circadian variations (P<0.0001), with the greatest day to night variation seen in normals, the least in diabetics, and intermediate values in chronic angina. These changes in heart rate variability circadian rhythms reflect significant reductions in cardiac parasympathetic activity with the most marked reduction in nocturnal vagal activity. Given the circadian pattern of myocardial ischemia and infarction, these data suggest that quantification of the magnitude of circadian variation in heart rate variability may have the potential to further risk stratify chronic angina and diabetes for future cardiac events.
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PMID:Circadian patterns of heart rate variability in normals, chronic stable angina and diabetes mellitus. 1052 63

Fasting and postglucose hyperinsulinemia are recognized risk factors for acute coronary events. The insulin reactivity of patients with acute coronary syndromes, however, has not been carefully compared with that of patients with chronic stable angina. We used Bergman's minimal model to analyze the insulin response to intravenous glucose in 21 subjects: 8 patients with previous (>3 months) acute coronary syndrome but no effort-related angina; 6 patients with stable effort angina but no prior acute event; and 7 healthy controls. Diabetes mellitus, systemic hypertension, dyslipidemias, and obesity were excluded. All patients underwent coronary angiography. Insulin sensitivity, glucose effectiveness, and glucose tolerance were determined from insulin and glucose concentrations measured frequently up to 3 hours after a 0.33 g/kg intravenous glucose bolus. Patients with previous unstable angina or acute myocardial infarction had less extensive disease at angiography than patients with stable angina (p = 0.007). Both patient groups had higher basal and 180-minute insulinemia than controls (p <0.0007). However, patients with stable angina did not differ significantly from controls with regard to early and late insulinemic response to glucose. In contrast, patients with previous acute onset of ischemia had significantly greater 180-minute integrated insulinemia (p = 0.04) and reduced insulin sensitivity (p = 0.05) after the glucose challenge than did the stable angina group. These data suggest that patients with acute presentation of coronary artery disease, compared with patients with uncomplicated chronic stable angina, have an impaired insulin response to glucose despite less extensive coronary disease at angiography.
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PMID:Comparison of insulin response to intravenous glucose in healed myocardial infarction, in "cooled-off" unstable and stable angina pectoris, and in healthy subjects. 1053 2

The prognostic significance of ambulatory ischemia, alone and in relation to ischemia during exercise was assessed in 686 patients (475 men) with chronic stable angina pectoris taking part in the Angina Prognosis Study In Stockholm (APSIS), who had 24-hour ambulatory electrocardiographic registrations and exercise tests at baseline (n = 678) and after 1 month (n = 607) of double-blind treatment with metoprolol or verapamil. Ambulatory electrocardiograms were analyzed for ventricular premature complexes and ST-segment depression. During a median follow-up of 40 months, 29 patients died of cardiovascular (CV) causes, 27 had a nonfatal myocardial infarction, and 89 underwent revascularization. Patients with CV death had more episodes (median 5 vs. 1; p<0.01) and longer median duration (24 vs. 3 minutes; p<0.01) of ST-segment depression than patients without events. For those who had undergone revascularization, the duration was also longer (12 vs. 3 minutes; p<0.05). In a multivariate Cox model including sex, history of previous myocardial infarction, hypertension, and diabetes, the duration of ST-segment depression independently predicted CV death. When exercise testing was included, ambulatory ischemia carried additional prognostic information only among patients with ST-segment depression > or =2 mm during exercise. When the treatment given and treatment effects on ambulatory ischemia were added to the Cox model, no significant impact on prognosis was found. Ventricular premature complexes carried no prognostic information. Thus, in patients with stable angina pectoris, ischemia during ambulatory monitoring showed independent prognostic importance regarding CV death. Ambulatory electrocardiographic monitoring and exercise testing provide complementary information, but only among patients with marked ischemia during exercise. Treatment reduced ambulatory ischemia, but the short-term treatment effects did not significantly influence prognosis.
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PMID:Prognostic implications of ambulatory myocardial ischemia and arrhythmias and relations to ischemia on exercise in chronic stable angina pectoris (the Angina Prognosis Study in Stockholm [APSIS]). 1056 22

Many important developments recently have been made in the treatment and prevention of coronary artery disease (CAD) in postmenopausal women. Substantial evidence supports focusing on comprehensive risk factor modification based on the "ABCs" of CAD management from the American College of Cardiology, the American Heart Association, and the American College of Physicians-American Society of Internal Medicine guidelines on chronic stable angina. This approach emphasizes cardiovascular risk factor interventions that include antiplatelet agents, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, cholesterol-lowering medications, diabetes control, and counseling on diet and exercise. Despite the expanding available literature, many questions on CAD in postmenopausal women remain unanswered and await the publication of ongoing and future research. The unexpected findings from the HERS (Heart and Estrogen/progestin Replacement Study) failed to show a benefit of hormone replacement therapy (HRT) in reducing the risk of subsequent events in postmenopausal women with CAD, and instead reported an early increase in CAD events. Based on the data available so far, we advise against starting HRT in postmenopausal women with a recent coronary event for the sole purpose of CAD prevention. For women with acute coronary syndromes, prompt angiography and revascularization should be considered.
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PMID:Coronary Artery Disease in Postmenopausal Women. 1113 91

Patients with suspected chronic stable angina can be evaluated in three stages. In stage one, the clinician uses information from the history, physical examination, laboratory tests for diabetes and hyperlipidemia, and resting electrocardiography to estimate the patient's probability of coronary artery disease (CAD). In stage two, additional testing for patients with a low probability of CAD focuses on diagnosing noncoronary causes of chest pain. Patients with a high probability of CAD have stress tests to assess their risk from CAD, and patients with an intermediate probability of CAD have stress tests to estimate the probability of CAD and assess their risk from CAD. Most patients with new-onset angina can start stress testing with exercise electrocardiography. The initial stress test should be a stress imaging procedure for patients with rest ST-segment depression greater than 1 mm, complete left bundle-branch block, ventricular paced rhythm, preexcitation syndrome, or previous revascularization with percutaneous coronary angioplasty or coronary artery bypass grafting. Patients who cannot exercise can have an imaging procedure with stress induced by pharmacologic agents. In stage three, patients with a predicted average annual cardiac mortality rate between 1% and 3% should have a stress imaging study or coronary angiography with left ventriculography. Those with a known left ventricular dysfunction should have cardiac catheterization. Patients with CAD who have an estimated annual mortality rate greater than 3% should have cardiac catheterization to determine whether their anatomy is suitable for revascularization. Patients with an estimated annual mortality rate less than 1% can begin to receive medical therapy.
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PMID:Guidelines for the management of patients with chronic stable angina: diagnosis and risk stratification. 1157 57


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