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

A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension. Hyperinsulinemia has been recognized as a major risk factor for the development of coronary artery disease independent of blood pressure and plasma lipid levels. All these conditions are frequently associated, particularly in aging, a state itself characterized by hyperinsulinemia. This common association has prompted the hypothesis that hyperinsulinemia may be a causative factor rather than the consequence of obesity, diabetes, hypertension, and hyperlipidemia. If that is the case, defining the nature and mechanisms of hyperinsulinemia becomes of primary interest. Insulin resistance is also a striking feature of all of the above mentioned pathologic states. In the presence of a preserved B-cell function, hyperinsulinemia can represent the mechanism designed to overcome the defect in the biological action of the hormone. For instance, there is a clear-cut age-related decline in the body's sensitivity to insulin. In order to compensate for this defect in insulin-mediated glucose metabolism, the B-cell must increase its secretion. On the other hand, a certain degree of insulin resistance can be induced both in animals and man by prolonged euglycemic hyperinsulinemia. Little is known regarding possible primary defects of the B-cell leading to uncontrolled oversecretion of insulin and subsequent insulin resistance. The primary defect, more probably, resides in an alteration of one or more of the steps whereby insulin exerts it own action. In favor of this hypothesis are the observations that insulin resistance segregates in familial clusters and that the first defect found in normoglycemic relatives of insulin-resistant diabetic patients is a reduced transformation of glucose into glycogen. Whatever is the primary defect, it is likely that a correction of insulin resistance might reduce the circulating levels of plasma insulin, possibly playing a beneficial effect on glucose tolerance, body weight, blood pressure and plasma lipid concentration.
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PMID:[Hyperinsulinism. Causes and mechanisms]. 133 21

A number of risk factors/indicators for cardiovascular disease, mainly stroke and coronary artery disease, have been established. Most powerful among the traditional risk factors are hypertension, cigarette smoking and elevated serum cholesterol. All three can successfully be modified by therapeutic intervention, which in turn will result in reduced risks. In recent years several novel risk indicators have been identified. The most powerful of these appears to be increased left ventricular mass, particularly when diagnosed with echocardiographic technique. Again, it is possible to reduce this risk factor, for instance by antihypertensive therapy, but the independent risk reduction attributable to this manoeuvre remains to be determined. Other novel risk indicators are male type adipose distribution, reduced insulin sensitivity and a number of newly detected lipoprotein fractions. At present little is known about the value of intervention against these factors in terms of risk reduction. It can be concluded that a structured concerted effort at reducing established risk factors such as arterial hypertension, elevated serum cholesterol and cigarette smoking is desirable for forming the basis of preventive strategies in cardiology. As regards some of the novel risk indicators, some of which appear more powerful than the old established ones, further research is needed before a clear opinion can be formulated regarding the value of intervention.
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PMID:The key issues in preventive cardiology. 134 36

The results of epidemiologic studies on the efficacy of different strategies of prevention or improvement of the prognosis of coronary artery disease are generally expressed in terms of percentage reduction of risk; for example, the treatment of hypercholesterolaemia reduces the risk of coronary death by 21%. In order to improve the assessment of the efficacy of these approaches the authors propose to take into account the number of subjects which needs to be treated each year to prevent one cardiovascular event more than the control group (for example, in hypercholesterolaemia, 1,736 patients). This number depends on the reduction of risk and also on the incidence of complications in the control group. Using this method, the authors classified different therapeutic strategies in order of their efficacy: thrombolytic therapy in the acute phase of myocardial infarction, then aortocoronary bypass grafting of left main coronary or triple vessel disease, secondary prevention with stopping smoking, and betablocker therapy. Finally, primary prevention with anti-smoking campaigns, treatment of hypertension and hypercholesterolemia. Based on this figure and knowing the annual cost of patient treatment, it is possible to calculate a cost-effectiveness ratio for each of these therapeutic interventions.
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PMID:[How to evaluate the cost/effectiveness ratio of different therapies of coronary disease]. 134 16

There is considerable evidence that on the anterior surface of the heart (which is usually supplied by the left anterior descending and the proximal part of the left circumflex coronary arteries), sympathetic efferent reflexes characterized by tachycardia and/or hypertension predominate following experimental or pathological perturbations. These cardiovascular reflexes are accompanied by an increase in presumed nociceptive afferent traffic and, in pathological condition, by pain. In these experiments, there is generally no effect of vagotomy on afferent nerve traffic, and lower cervical and upper thoracic sympathectomies help provide relief from angina. On the other hand, experimental or pathological perturbations involving the inferior-posterior surface of the heart (supplied by the right and distal parts of the left circumflex coronary arteries), are characterized by vagal efferent reflexes, resulting in bradycardia and/or hypotension. These reflexes are accompanied by an increase in vagal afferent nerve traffic and, in pathological conditions, by pain. In these experiments, vagotomy generally abolishes such cardiovascular reflexes, and lower cervical and upper thoracic sympathectomies are not effective in the relief from angina. Although cardiac sympathetic afferents are unquestionably involved in the central transmission of nociceptive information from the heart, it is also likely that there is a contributing role from the vagus in cardiac pain. It is important experimentally to understand the natural stimulus that gives rise to angina. In the clinical situation, a decrease in coronary blood flow or an increase in the metabolic demands of the myocardium due to increased work are obvious precipitating factors which lead to myocardial ischemia. In the experimental situation, occlusion of the coronary arteries is often used as a stimulus which mimics myocardial ischemia. As people who frequently experience angina have varying degrees of coronary artery disease, it is difficult to accept that the state of the coronary arteries of the normal experimental animal bear any resemblance to the state of the coronary arteries under pathological conditions. That is, the gain of homeostatic reflexes, the basal concentrations of neuroactive substances in the plasma, the myocardium and the afferent terminals, the excitability of the afferents, access of chemical mediators (e.g. bradykinin, 5-HT, adenosine, histamine, prostaglandins, potassium, lactate), to afferents, and the overall function of the animal are all significantly different. We have no idea how control mechanisms have been altered in the person with severe coronary artery disease compared to the normal patient or the "normal" experimental animal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A critical review of the afferent pathways and the potential chemical mediators involved in cardiac pain. 135 Dec 70

Coronary artery disease accompanied by symptomatic and asymptomatic myocardial ischemia is a common entity in older patients. The pathophysiology of myocardial ischemia is related to an imbalance in myocardial demand and coronary perfusion. Treatment strategies for symptomatic myocardial ischemia include correction of aggravating medical conditions (eg, anemia or hypertension) and the use of nitrates, beta-adrenergic blockers, salicylates, and calcium-entry blockers, alone or in combination. Silent myocardial ischemia is also a prevalent condition in older individuals, with and without angina pectoris. Treatment regimens are similar to those used in symptomatic patients.
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PMID:Angina pectoris and silent ischemia in the elderly: a management update. 135 66

Hypertension is a known risk factor in the genesis of coronary artery disease. However, the effect of pre-existing hypertension on the long-term mortality in patients with established coronary heart disease is not clear. The present cohort study analysed the influence of baseline mild to moderate treated hypertension in cases of known coronary heart disease with cardiac mortality as end point. Data from a cohort of 511 patients including 266 normotensives and 245 controlled hypertensives was analysed over a follow-up period of 9 to 11 years. The baseline data were identical regarding other major risk factors like age, gender, smoking, diabetes, cholesterol levels and congestive heart failure on univariate analysis. There were more cases of myocardial infarction in the normotensive group. The number of patients receiving beta-blockers or aspirin were similar in both groups. However, more patients in the hypertensive group received nifedipine. Actuarial analysis of survival showed that mortality was the same in both groups with an overall cardiac mortality of 65 (26.5%) in the hypertensive group and 86 (32.3%) in the normotensive group (P greater than 0.1). The survival curves also showed no significant difference in mortality at any point in time (logrank test = 2.37, P greater than 0.1). Analysis of mortality after adjusting for myocardial infarction at first presentation also showed no significant difference. These data indicate that in patients with coronary heart disease the presence of mild to moderate hypertension does not add to the risk of cardiac mortality.
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PMID:Influence of mild to moderate treated hypertension on 9-11 year mortality in patients with pre-existing coronary heart disease. 135 40

Aerobic exercise may prevent hypertension and reduce blood pressure and mortality in hypertensive patients and those at high risk for coronary artery disease. Supervised aerobic exercise at an intensity of 70% to 80% of maximal aerobic capacity is recommended to achieve cardiovascular conditioning and other health benefits. When antihypertensive drug therapy is required, physicians should choose an agent that has favorable secondary effects, including hemodynamic responses to exercise. The most favorable effects are achieved with calcium channel blockers, angiotensin-converting enzyme inhibitors, alpha blockers, and central alpha agonists. The effects of diuretics are less desirable, and beta blockers should be a last choice for hypertensive patients who are physically active.
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PMID:Exercise and hypertension. Maximizing the benefits in patients receiving drug therapy. 135 18

In patients ranked ASA 1, laryngoscopy and intubation lead to an average increase in blood pressure of 40 to 50%, and a 20% increase in heart rate. These changes, which are greatest one minute after intubation, last for 5 to 10 min. They are due to sympathetic and adrenal stimulation, which may also result in some arrhythmias. About half the patient with coronary artery disease experience episodes of myocardial ischaemia during intubation when no specific prevention is undertaken. Among the different means available for this, narcotics seem to have a reliable and constant effect, but they may be responsible for postoperative respiratory depression. The protective effect of fentanyl starts at 2 micrograms.kg-1, and is at a maximum at 8 micrograms.kg-1. Lidocaine is the drug used most. Recent studies have questioned its efficacy. In clinical practice, it is particularly effective in preventing the pressor response to tracheal intubation, whatever its route of administration (intravenous or intratracheal), but not the increase in heart rate. Beta blockers with bradycardic, antihypertensive, antiarrhythmic and antiischaemic properties, have been advocated. As opposed to lidocaine, these agents are more effective in preventing the changes in heart rate than the pressor response. Because of their depressor effect on the myocardium, their place still remains to be defined, especially in the cardiac risk patient. Short-acting beta blockers should be preferred. Nitroglycerin is specifically indicated in coronary artery disease. Other agents, such as clonidine or calcium blockers, seem to be less effective or less convenient in preventing the haemodynamic alterations. In clinical practice, prevention will first rely on a sufficient dose of narcotics. In some cases, nitroglycerin or beta blockers may be used so as to decrease the doses of narcotics, without altering their efficacy; however, the risk of hypotension should be constantly borne in mind. If preventing measures have not been taken, short-acting antihypertensive agents (beta blockers, calcium blockers) should be used in patients who develop major hypertension during laryngoscopy and intubation.
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PMID:[Consequences and prevention methods of hemodynamic changes during laryngoscopy and intratracheal intubation]. 135 16

The incidence of hypertension and coronary artery disease among diabetic patients is approximately two to three times greater than in nondiabetics. Recent evidence suggests that even moderately elevated blood pressure levels may result in diabetic complications involving the eyes or kidneys. However, treatment of diabetic patients with antihypertensive drugs may have a deleterious metabolic effect. Previous studies have suggested that calcium antagonists may reduce insulin secretion and therefore impair glucose tolerance. This has not been substantiated clinically; in general, it would appear that calcium antagonists have a minimal hyperglycemic effect. To establish whether interruption of excitation-contraction coupling in arterial smooth muscle and altered stimulus-secretion coupling occur at pharmacologically equivalent doses of calcium antagonist, the effect of nicardipine on insulin output and vascular resistance was studied in the isolated perfused rat pancreas and in eight hypertensive patients with impaired glucose tolerance during oral glucose tolerance testing (OGTT). Baseline insulin output in vitro was 86 +/- 22 ng/min at 8.0 mM glucose and 2.5 mM calcium. Application of 10 nM nicardipine reduced insulin output to 86% of baseline, whereas output was reduced to 16% by 1 microM nicardipine and to 6% by 10 mM nicardipine. Changes in duodenopancreatic outflow indicated maximal vasodilation of the pancreas at all three concentrations of nicardipine (10 nM-10 mM). In vivo nicardipine 30 mg t.i.d. for 2 weeks reduced systolic blood pressure from 168 +/- 2 mm Hg to 136 +/- 4 mm Hg (p < 0.001) and diastolic blood pressure from 96 +/- 3 mm Hg to 78 +/- 2 mm Hg (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical effects of calcium antagonists in hypertensive diabetics. 136 2

Epidemiological studies indicate that there are biological interrelationships between blood pressure and blood lipids that may influence the mechanisms whereby hypertension is associated with an increased risk of coronary artery disease. Serotonin (5-HT) and thromboxane A2, which are released from aggregating platelets, mediate platelet-induced vasoconstriction, which itself significantly contributes to coronary artery constriction in vivo. Platelet aggregatory response to serotonin is modulated by disparate effects of lipoprotein fractions. This corresponds to the recognized differences in degree of atherogenicity of low- (LDL) and high-density lipoprotein (HDL). Amplification of serotonin-induced platelet aggregation by LDL and its inhibition by HDL support the hypothesis that 5-HT-mediated effects represent a mechanism clinically relevant to both chronic progression of atherosclerosis (particularly at sites of vascular injury and atherosclerotic plaques) and acute thrombotic events. Calcium antagonists differ in their platelet-inhibition potency, including their effects on platelet response to 5-HT and LDL. Verapamil and isradipine inhibit platelet aggregation induced by 5-HT at therapeutic concentrations. Isradipine also inhibits the amplifying effect of LDL on 5-HT-induced aggregation. These platelet effects of calcium antagonists appear to be neither group- nor class-specific but, rather, drug-specific.
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PMID:Platelet activation by low-density lipoprotein and serotonin: effects of calcium antagonists. 137 30


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