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2.
Can J Cardiol ; 6(8): 367-72, 1990 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-2148501

RESUMO

Some old icons of hypertension warrant questioning in view of new insights. Lowering of blood pressure is no criterion of efficacy in prevention of cardiovascular morbidity, mortality and sudden death. The drugs used in early studies - diuretics, vasodilators and reserpine - greatly improved mortality from malignant hypertension, apoplectic stroke and congestive heart failure, but had little or no effect in persons with milder degrees of elevated blood pressure, who constitute the vast majority of hypertensives. The failure of diuretics and vasodilators to influence cardiovascular disease favorably appears due not to their known adverse effects on risk factors, such as lipids, as some have held, but to a failure - in conjunction with some sympathetic blocking agents - to cause effective regression of left ventricular hypertrophy, the keystone of successful therapy. A study of 674 hypertensive persons surveyed in the United States and eastern Canada, personally examined during their visit to a Florida health resort, has shown striking changes in prescribing practice during the period surveyed (1985-88), notably with increased use of angiotensin converting enzyme (ACE) inhibitors and, to a lesser degree, increased use of calcium channel blockers. Both of these cause regression of left ventricular hypertrophy, and will hopefully show long term benefit in decreasing hypertension mortality. Left ventricular hypertrophy is detected most sensitively echocardiographically, and is worthwhile not only for estimation of prognosis, but also for guiding therapy. Left atrial hypertrophy is a mirror of left ventricular hypertrophy and may be detected echocardiographically and in the electrocardiogram.(ABSTRACT TRUNCATED AT 250 WORDS)


Assuntos
Cardiomegalia/tratamento farmacológico , Hipertensão/tratamento farmacológico , Cardiomegalia/complicações , Humanos , Hipertensão/complicações
3.
Artigo em Inglês | MEDLINE | ID: mdl-2353405

RESUMO

Joint studies of the ALIMDA and Society of Actuaries, notably those of 1935, 1959 and 1979, established that there is a progressive rise in cardiovascular mortality with successive increments in blood pressure. This has provided the basis of underwriting. The converse is not true, or at least has not been true until very recently. Drugs that effectively reduce blood pressure have been available for several decades, but reduction and maintenance of blood pressure is still accomplished in only a minority of hypertensives. Long-term trials employing a combination of drugs, i.e., diuretics, vasodilators and reserpine and subsequently beta-blockers, almost without fail have not shown that treatment with these agents significantly reduces heart disease mortality and sudden death. This has been attributed, perhaps without basis, to an unfavorable countering effect of increased lipid levels, aggravating this risk factor, and other undesirable metabolic effect of diuretics, such as hypokalemia and depletion of body magnesium, increasing the propensity to ventricular arrhythmias, hyperglycemia, worsening diabetes, and hyperuricemia. A survey of 674 persons with hypertension seen personally during the period 1985-89, who were under the care of approximately that many physicians, reveals striking changes in drug prescription and use during this brief period that portend a major change in the outlook of hypertension. Two classes of drugs have increased rapidly in popularity: these are the angiotensin-converting enzyme inhibitors (ACE inhibitors) and the calcium blockers. Both classes of drugs effectively lower blood pressure and have minimal side effects with good compliance. They act not only to reduce peripheral vascular resistance, but also locally in the heart muscle to directly cause left ventricular hypertrophy to regress, an effect of great consequence. The drugs used in former trials such as the vasodilators and diuretics have no effect on left ventricular hypertrophy, unlike the ACE inhibitors and calcium antagonists. Left ventricular hypertrophy is the key lesion in hypertension and is only in part due to increased work load imposed by elevated pressure. It is associated with elevated blood pressure, but not closely and occurs independently; ventricular myocytes as well as myocytes of the vasculature being stimulated to growth by angiotensin and calcium, potentiating the effect of norepinephrine. Left ventricular hypertrophy greatly increases the propensity to ventricular arrhythmias and sudden death, and is a prime cause of cardiac mortality and sudden death not only in hypertension, but also in obesity, aging and diabetes, in which conditions left ventricular hypertrophy also is very common.(ABSTRACT TRUNCATED AT 400 WORDS)


Assuntos
Anti-Hipertensivos/uso terapêutico , Hipertensão/tratamento farmacológico , Adulto , Idoso , Idoso de 80 Anos ou mais , Eletrocardiografia , Feminino , Humanos , Hipertensão/diagnóstico , Hipertensão/mortalidade , Masculino , Pessoa de Meia-Idade
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