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The relationship between cerebro-cardiovascular events (CCE) and work-related factors was examined in a cohort of 899 treated hypertensive men who were aged 50-59 yr and working more than 7 portal to portal hours (PPH). During the follow-up of 2.8 yr (2,513 person-years), 27 cases of CCEs occurred, which were classified into 18 cases of stroke, 7 cases of acute myocardial infarction, and 2 cases of others. Using univariate analysis, it was found that managerial position and long PPH (more than 11 h) were significantly related to CCE (relative risk of 3.0 and 2.2, respectively) as well as risk factors such as emaciation, left ventricular hypertrophy, excessive sleeping hours, obesity, cigarette smoking, and inadequate control of systolic blood pressure. Using Cox proportional hazards general model, both managerial position and long PPH remained independently related to the risk of CCE (hazards ratio and 95% confidence interval, 4.1; 1.7-10.0 and 2.7; 1.1-6.2, respectively), after adjustment for other risk factors. These findings suggested that work-related factors, such as managerial position and long PPH, are independent risk factors of CCE among treated hypertensive male workers in the fifth decade.
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PMID:[Risk factors of cerebro-cardiovascular events in treated hypertensive male workers in the fifth decade]. 151 87

Over the past decade we have seen a shift in the strategy for the treatment of hypertension, from stepped therapy--involving a highly structured, unvarying series of steps--to recommendations for more individualized treatment. How shall we accomplish that goal? Severe hypertension provides a clear indication to bypass earlier recommendations. Demographic data such as age, gender, and race, often cited, have proved less helpful. Concomitant medical problems, which are found in greater than 50% of hypertensive patients, are most often the crucial determinants in the selection of antihypertensive therapy. Concurrent coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, chronic obstructive pulmonary disease, borderline cognitive dysfunction, anxiety, and depression are all common. Each has implications for antihypertensive therapy. Moreover, blood pressure reduction is a surrogate for our real goal, which is reduction of cardiovascular risk. Thus, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, hyperlipidemia, and insulin resistance as additional risk factors in hypertension. Consideration of all of these factors makes it possible to individualize antihypertensive therapy in most patients.
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PMID:Evolution of the treatment of hypertension: what really matters in the 1990s? 151 35

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

Hypertension and obesity are closely related. Obese patients tend to have increased intravascular volume and cardiac output and decreased total peripheral vascular resistance and plasma renin activity. Lean patients with essential hypertension usually have increased total peripheral resistance. Left ventricular adaptation in obesity consists of eccentric left ventricular hypertrophy (LVH), regardless of the level of arterial pressure. Obesity and hypertension occurring together place a dual burden on the left ventricle and are associated with systolic and diastolic dysfunction, lipid abnormalities, insulin resistance, and a propensity for frequent, complex ventricular arrhythmias. Congestive heart failure and sudden death are common sequelae of obesity-hypertension and LVH. Treatment should include vigorous efforts at weight reduction and sodium restriction. Diuretics are ideal agents from a hemodynamic standpoint but often do not improve the total risk profile, with the possible exception of indapamide (Lozol). Calcium blockers may be ideal agents because of their favorable effects on both hemodynamics and total cardiovascular risk profile.
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PMID:Left ventricular hypertrophy. Its relationship to obesity and hypertension. 153 69

A major concern with the use of starvation or semistarvation diets for weight reduction in severely obese people has been the reports of sudden death due to ventricular arrhythmias. Obesity per se is associated with cardiovascular changes, including left ventricular hypertrophy and prolongation of the QT interval. With weight loss, the mass of the heart and left ventricle decrease, but some signs of left ventricular dysfunction remain. The effect of weight loss on the electrocardiogram abnormalities of obesity appears to depend upon diet duration and upon whether protein and mineral nutritional status is maintained. Copper, potassium, and magnesium deficiencies may play important roles in promoting an electrically unstable heart. Stress, by eliciting autonomic imbalance, may act upon an electrically unstable heart to provoke acute arrhythmias in a subset of the obese population with QT interval prolongation.
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PMID:Cardiac effects of starvation and semistarvation diets: safety and mechanisms of action. 153 77

Blood pressure reduction in hypertensive patients is a surrogate for the real therapeutic goal of reducing the risks consequent to hypertension. This surrogate is convenient but its use may have important therapeutic implications. Results of treatment with new antihypertensive agents, data from clinical trials, and insights into underlying mechanisms are reviewed. The overall success of antihypertensive therapy has been undeniable, but has reduced minimally the frequency of atherosclerosis and coronary events; metabolic disarray resulting from the agents used, especially thiazides and beta blockers, may have contributed to this. Electrolyte abnormalities predispose to malignant arrhythmias and sudden death during myocardial infarction. Left ventricular hypertrophy, a chief risk factor for coronary events, arrhythmias, and heart failure, responds selectively to antihypertensive agents. Similarly, progression of renal injury may be sensitive to the agents used. Obesity and hypertension frequently coexist. Evidence is growing that atherogenic abnormalities common in obese patients, such as insulin resistance, also occur in the nonobese patient and are sensitive to the antihypertensive agent selected.
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PMID:Management of hypertension and cardiovascular risk. 167 28

Obvious, but often forgotten, is the premise that blood pressure reduction in the patient with hypertension is a surrogate for our real goal, which is reduction in the risks consequent to hypertension. This surrogate, a convenience for regulatory agencies, has therapeutic implications. As the array of antihypertensive agents available has grown, along with information from clinical trials and insights into underlying mechanisms, it has become reasonable to examine that premise. The overall success of antihypertensive therapy has been undeniable, but has not influenced the advance of atherosclerosis, primarily coronary events. Multiple observations suggest that metabolic disarray consequent to the use of antihypertensive agents, especially thiazides and beta-blockers, may have contributed to this scenario. Electrolyte abnormalities predispose to malignant arrhythmias and sudden death during myocardial infarction. Left ventricular hypertrophy, a major risk factor for coronary events, arrhythmias, and heart failure, responds selectively to antihypertensive agents. Similarly, the progression of renal injury in the hypertensive patient may be sensitive to the agents employed. Obesity and hypertension coexist frequently; moreover, evidence is growing that atherogenic abnormalities common in the obese patient, such as insulin resistance, not only occur frequently in the nonobese patient, but are also sensitive to the antihypertensive agent selected. Although predictions are risky, it seems safe to predict that the next chapter in antihypertensive therapy will examine whether we need to go beyond blood pressure reduction in selecting such therapy.
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PMID:Management of hypertension: considerations involving cardiovascular risk reduction. 169 35

Left ventricular hypertrophy (LVH), an increase in the muscle mass of the left ventricle, has been identified as a powerful risk factor for future cardiovascular morbidity and mortality. The risk of acute myocardial infarction, congestive heart failure, sudden death, and other cardiovascular events increases six- to eightfold with the presence of LVH. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left ventricular filling and contractility. Hypertension, obesity, advanced age, valvular heart disease, and other disorders that cause an increase in the hemodynamic burden can lead to LVH. Left ventricular hypertrophy and its sequelae can be reduced by specific antihypertensive therapy but, despite these promising findings, future epidemiological studies are necessary to document the clinical benefits of a reduction of LVH.
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PMID:Left ventricular hypertrophy: an independent risk factor. 172 10

Exogenous obesity is characterized hemodynamically by expanded intravascular (plasma) volume associated with an increased cardiopulmonary volume and cardiac output. In contrast, essential hypertension is related to an increased total peripheral resistance that is more or less uniformly distributed throughout the component organ circulations associated with a contracted plasma volume in proportion to the height of arterial pressure. Thus, both cardiac output and total peripheral resistance are elevated in obesity hypertension, and both impose a load on the left ventricle, resulting in both a volume and a pressure overload left ventricular hypertrophy. Although renal vascular resistance is not as increased as it is in lean hypertensive patients, these patients are subjected to hyperfiltration and proteinuria. Additionally, these hemodynamic alterations coexist with carbohydrate intolerance, hyperinsulinemia, hyperlipidemia, and hyperuricemia. With weight reduction and associated pressure reduction, the hemodynamic and metabolic changes reverse toward normal. However, should this not be achievable, the angiotensin converting enzyme inhibitors and calcium antagonists provide rational physiological approaches to drug therapy. With these agents pressure reduction is achieved through a fall in vascular resistance without intravascular volume expansion, and this is associated with reduced left ventricular mass and preserved cardiac and renal function, and without exacerbation of preexisting metabolic perturbations. Hence, these two classes of antihypertensive agents may provide a rational and physiological means for reversing the pathophysiological alterations of hypertensive disease in those obese patients in whom weight control is not possible.
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PMID:Obesity hypertension. Converting enzyme inhibitors and calcium antagonists. 173 Apr 48

Severe obesity is associated with abnormalities of cardiac structure and function. These include an increased cardiac workload and ventricular hypertrophy. Hypertension in combination with severe obesity seriously burdens the heart because the increased preload and afterload compound cardiac work. Weight reduction induced by gastric operations for severe obesity is associated with resolution of hypertension, reduction in ventricular wall thickness and cardiac chamber size, as well as improved systolic function. Additional data are needed to predict when in the course of development of obese cardiomyopathy the changes in contractile function become irreversible. Additionally, the impact of coronary artery disease on the progression of obese cardiomyopathy and the effects of surgical weight reduction on cardiac structure and function need to be further clarified. Studies of the association between obesity, its treatment, and modification of cardiovascular risk are a major focus of preventive cardiology today.
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PMID:Heart disease and hypertension in severe obesity: the benefits of weight reduction. 173 33


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