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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The calcium channel blocking agents have multiple hemodynamic effects that make them potentially valuable in treating many cardiovascular disorders. They are potent dilators of coronary and peripheral arteries and in isolated tissue preparations exert potent negative inotropic, chronotropic, and dromotropic effects. In intact animals the peripheral arterial vasodilatation induces reflex-mediated adrenergic activity, which opposes the direct negative inotropic, chronotropic, dromotropic, and hypotensive effects. The individual calcium channel blockers have different relative potencies on various cardiovascular functions. The net hemodynamic and electrophysiologic effect of each agent, therefore, results from a complex interplay of direct and reflex phenomena. The clinical efficacy of these agents in classic angina pectoris relates to their ability to decrease afterload, myocardial contractility, and heart rate and increase coronary blood flow. The agents have been used to prevent coronary spasm in Prinzmetal's variant angina. The negative inotropic effects of verapamil are valuable in improving the symptoms and hemodynamic disturbances of hypertrophic cardiomyopathy. The role of these agents in treating arterial hypertension, unstable angina pectoris, acute myocardial infarction, and ischemia during cardiopulmonary bypass needs to be determined.
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PMID:Calcium channel blocking agents in the treatment of cardiovascular disorders. Part II: Hemodynamic effects and clinical applications. 700 93

There is an abundance of information suggesting that prostaglandins are involved in the development and clinical expression of atherosclerosis. Many studies demonstrate a relationship between prostaglandins and the risk factors for peripheral and coronary artery disease. Thus, part of the mechanism by which hyperlipidemia, diabetes mellitus, smoking, hypertension, sex hormones, age, heredity, emotional stress and diet contribute to the development and progression of atherosclerosis may be through an imbalance between thromboxane A2 and prostaglandin I2. Recent studies show a temporal relationship between acute ischemic events (specifically, unstable angina) and a transcardiac increase in thromboxane B2, while others demonstrate a salutary effect of disaggregatory and vasodilatory prostaglandins in such patients. If prostaglandins and thromboxane prove important in ischemic vascular disease, attention will be directed at the correction of their pathologic imbalance. This may be accomplished by dietary manipulation as well as by the development of prostaglandin receptor antagonists or inhibitors of specific prostaglandin pathways.
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PMID:Prostaglandins and ischemic heart disease. 703 86

Malondialdehyde (MDA), a product of platelet lipid peroxidation, was measured in human platelet-rich plasma. Levels of 3.19 n moles/10(9) platelets /+- 0.40 S.E. in 11 patients with prosthetic heart valves were elevated (p < 0.25) compared to 17 normal subjects (2.09 /+- 0.13 n moles/10(9) platelets). Reduced production (1.44 /+- 0.28 n moles/10(9) platelets, p < 0.5) was found in 10 patients with unstable angina. Normal levels were found in patients with mitral stenosis, cardiomyopathy or hypertension. Usual serum levels of drugs used in cardiac treatment reduced MDA levels as follows: acetaminophen, 47% (p < .01); aspirin, 58% (p < .05); furosemide, 32.6% (p < .005), and sulfinpyrazone, 41% (p < .05). Digoxin, dipyridamole, heparin, hydrochlorothiazide, lidocaine, nitroglycerin, procainamide, propranolol, quinidine, or warfarin had no significant effect at therapeutic concentrations. None of the drugs explained the enhanced production in patients with prosthetic valves while enhanced production in patients with prosthetic valves while analgesic therapy could explain the decreased levels in other cardiacs. The half-time of platelet survival, measured by suppression of malondialdehyde production, was 3.2 /+- 0.24 days in 9 normal subjects but could not be measured reliably in most patients because of multiple drug therapies. We conclude that the blood platelets of patients with prosthetic heart valves differ from those of normal subjects in their capacity to release malondialdehyde after stimulation with n-ethylmaleimide. Additionally, we find that inhibition of malondialdehyde production by several pharmacologic agents limits the usefulness of this method for the measurement of platelet survival in cardiac patients.
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PMID:Platelet malondialdehyde in cardiovascular disease: effect of prosthetic heart valves and cardioactive drugs on production. 745 95

Although small body size and coronary artery diameter are recognized as major contributors to the increased risk of coronary artery bypass grafting in women, few studies have established the independent influence of body size and gender on outcome. We studied 7025 consecutive patients (5694 men, 1331 women) undergoing isolated coronary artery bypass grafting between 1990 and 1994. Women were older, had higher preoperative prevalences of urgent operation because of unstable angina, diabetes, peripheral vascular disease, hypertension, and single-vessel coronary artery disease (p < 0.0001), and a lower prevalence of left ventricular ejection fraction 40% or less (p < 0.0001). The prevalences of operative mortality (men, 1.8%; women, 3.5%), low-output syndrome (men, 6.6%; women, 14.8%), and myocardial infarction (men, 2.8%; women, 5.5%) were higher in women (p < 0.0001). Patients were divided into quartiles for body surface area, weight, height, and body mass index. For both men and women, there was no difference in operative mortality between the highest and lowest quartiles of body size. Women, however, had a higher prevalence of operative mortality than men in the lower quartiles of body surface area, height, and weight and in the higher quartiles of body mass index. Among men, the prevalence of low-output syndrome increased (p < 0.0001) with decreasing body surface area, weight, and body mass index, suggesting that body size did influence the prevalence of low-output syndrome. However, women had a higher prevalence of low-output syndrome than men in every category and quartile of body size (p < 0.0001). Multivariable analysis identified gender as a significant determinant of operative mortality (odds ratio 1.83, 95% confidence interval 1.27 to 2.64) and low-output syndrome (odds ratio 2.52, 95% confidence interval 2.05 to 3.11). When multivariable adjustments were made for body size and preoperative risk factors, gender remained a predictor of both operative mortality and low-output syndrome. Multivariable assessment of risk for men and women separately identified that urgent operation was a predictor of operative mortality (odds ratio 2.52, 95% confidence interval 1.32 to 5.61) and low-output syndrome (odds ratio 1.57, 95% confidence interval 1.14 to 2.17) in women but not men. In conclusion, the increased risk of coronary artery bypass grafting in women may be explained in part by dramatic differences in preoperative risk factors between men and women. In both men and women, small body size did not increase the risk of operative mortality, but may have contributed to the risk of low-output syndrome.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Is body size the cause for poor outcomes of coronary artery bypass operations in women? 747 87

Patients with coronary artery disease are particularly at risk perioperatively, as myocardial infarction, unstable angina, severe arrhythmia and cardiac death may occur. These events are often preceded by prolonged silent myocardial ischaemia (MI). Moreover, perioperative MI predicts long-term adverse cardiac outcome. Therefore, it is logical to prevent and treat MI. However, the detection of perioperative MI is difficult because of low sensitivity of ST-segment monitoring, low specificity of echocardiography and insufficient availability of equipment for its monitoring. A pragmatic approach is described, including preoperative consideration of myocardial revascularization prior to non-cardiac surgery and perioperative administration of antianginal agents; the effects of clonidine are discussed as well. The role of anaesthetic techniques and normovolaemic haemodilution is considered. MI episodes may be prevented or their duration may be shortened by treating tachycardia, hypotension and, possibly, hypertension. The risks of MI are particularly high during the postoperative period because increased global oxygen consumption associated with recovery, ventilator weaning, shivering and pain may lead to tachycardia and increased ventricular load. These factors must be taken into account in order to prevent MI and improve postoperative cardiac outcome.
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PMID:[Myocardial ischemia and anesthesia]. 748 76

The coexistence of different clinical syndromes due to atherosclerosis in different organs is not rare and emphasizes the diffuse nature of this vascular process. Although renovascular disease may cause hypertension and/or renal insufficiency, it may also occur in the absence of the usual clinical markers that suggest renovascular hypertension. We report a patient with stable coronary anatomy who presented with crescendo angina pectoris. Diagnosis of renovascular hypertension was made by screening renal angiography at the time of the cardiac catheterization. Renal artery stenting resulted in stabilization of the coronary syndrome and obviated the need for further coronary intervention. To our knowledge, this is the first case of renovascular hypertension precipitating an unstable coronary syndrome in a patient with documented stable coronary anatomy. Review of the literature supports that patients undergoing cardiac catheterization are a high risk population for renovascular disease, particularly in the presence of other predictive factors such as documented coronary artery disease, older age, female gender, congestive heart failure, peripheral vascular disease, renal insufficiency, and smoking. Firm recommendations for routine screening renal angiography in patients undergoing peripheral or coronary angiography will need further studies.
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PMID:Renal artery stenosis presenting as crescendo angina pectoris. 755 35

Hypoxia accompanying acute exposure to high altitude engenders augmented sympathetic nervous activity, thus increasing heart rate and blood pressure and the risk of effort angina and dysrhythmia in coronary patients. This risk is highest during the first 1 to 3 days and diminishes in 5 to 7 days as sympathetic activity subsides. Protective effects may result from 1. Gradual ascent. 2. Attention to blood pressure control. 3. Limitation of activity to less than the symptom-limiting degree at sea level, especially during the first 1 to 3 days. 4. Preexisting exercise tolerance of modest-to-moderate degree. 5. Ability of patient to appraise heart rate and blood pressure. Ascent by high-risk patients can be recommended to no more than moderate altitude, where adequate facilities for cardiovascular care are proximate. The risk of acute mountain sickness is not increased in older coronary patients. Strong contraindications to air travel by coronary patients would appear to be 1. New-onset angina. 2. Unstable angina. 3. Frequent or high-grade ventricular ectopy. 4. Severe or poorly controlled hypertension. Myocardial infarction within several weeks or months constitutes a relative contraindication, with persistent angina, ventricular ectopy, and poor ventricular function as the factors of greatest concern.
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PMID:Coronary problems associated with altitude and air travel. 761 18

To assess the clinical, coronary arteriographic, and hemodynamic differences between the unstable angina patients manifesting ST segment depression and those showing ST segment elevation as well as those demonstrating chest pain only without ST segment deviation during pacing, low-dose digital subtraction ventriculography was performed in 33 patients before and after abrupt cessation of atrial pacing during selective coronary arteriography. Transient ST segment depression during pacing was observed in 17 patients (52%), whereas 6 patients (18%) showed ST segment elevation; however, 10 patients (30%) did not manifest any ST segment deviation in spite of typical chest pain. Hypertension and a history of myocardial infarction were observed in a significantly higher (P < 0.05) proportion of patients with ST segment depression than in those with ST elevation. Patients who manifested ST segment depression during pacing had a higher incidence of triple-vessel disease (65 vs 17%; P < .05) as compared with the patients with ST segment elevation. Indirect evidence of intracoronary thrombi (complicated lesion, abrupt occlusion, and intraluminal filling defect) was noticed in a higher frequency (P < 0.05) in the group of patients with ST elevation during pacing. In patients with ST segment depression, no significant changes of global left ventricular (LV) functional parameters were observed. However, the length of the LV severe hypokinetic region was increased significantly (6.2 +/- 3.1 vs 23.5 +/- 6.2%; P < 0.005) during pacing in this group of patients. The shortening of the affected segments of the left ventricle was decreased significantly (52.3 +/- 3.6 vs 38.3 +/- 4.9%; P < 0.05) in these patients during pacing. In the group of patients with ST segment elevation during pacing, decrease in ejection fraction was associated with significant (P < 0.01) increase in midwall equatorial diastolic stress as compared with the patients with pacing-induced ST segment depression as well as patients without ST segment deviation. In the group of patients without ST segment deviation during pacing there was no considerable aggravation of LV global or regional function. This distinction should be taken into consideration in evaluating patients with unstable angina for diagnostic and therapeutic intervention.
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PMID:Pacing-induced ST segment deviation in patients with unstable angina: clinical, angiographic, and hemodynamic correlation. 761 59

Esmolol is a unique cardioselective, intravenous, ultra-short acting, beta-adrenergic blocking agent. A 9-minute half-life with rapid clinical onset and offset of action and the ability to titrate the drug to changing circumstances makes esmolol a useful addition to our treatment armamentarium. The efficacy and safety of esmolol have been shown in specific clinical settings, i.e. in patients with unstable angina, myocardial infarction, atrial fibrillation or flutter and supraventricular tachycardia. In the emergency management of hypertension, tachycardia or arrhythmia in critical care units, emergency room and surgery, esmolol is effective by attenuating hemodynamic responses from sympathetic activation or endogenous catecholamine release. With careful titration and monitoring of the patient, esmolol is relatively safe in the management of hypertension or tachyarrhythmias associated with congestive heart failure or chronic obstructive lung disease where beta-blockers are otherwise contraindicated. Different dosage schedules have been employed as per the clinical setting and the diagnosis. Generally, esmolol is infused intravenously in doses ranging from 25-300 micrograms/kg/min, along with a loading dose or bolus. The most frequently reported adverse effect associated with esmolol infusion was hypotension. Adverse effects due to beta-blockade can be corrected by down-titrating or discontinuing the infusion with complete disappearance of clinical effects in 20-30 minutes. Therefore, as an ultra-short acting beta-blocker, esmolol is an important therapeutic option in the acute clinical setting.
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PMID:Clinical rationale for the use of an ultra-short acting beta-blocker: esmolol. 762 Jun 91

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


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