Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic cough may be the sole presenting manifestation of bronchial asthma (reference 3; Corrao et al, 1979), and "cough variant asthma (CVA)" has been used to categorize such patients. In order to clarify the clinical picture of CVA, we evaluated the clinical history, laboratory data, sputum cytology and pulmonary function in 14 subjects (5 males and 9 females, aged 14 to 65 years) compatible with the following diagnostic criteria: (1) chronic cough persistent for more than 8 weeks, (2) no wheeze nor dyspnea, (3) no rales, (4) no past history of asthma, (5) bronchial hyperreactivity to methacholine proven by Takishima's method (reference 13), (6) effectiveness of bronchodilators against cough, (7) normal chest X-ray film, (8) afebrile and negative CRP, (9) absence of sinusitis and postnasal drip, or if present, they are proved not to be responsible for the cough, and (10) no other causes of cough such as heart disease, prescription of ACE inhibitors, current smoking. The results were as follows. 1) Many of the subjects were atopic, with positive skin tests to one or more common allergens in 10 subjects, elevated serum IgE in 4 subjects, and past history and family history of atopy in 4 and 7 subjects, respectively. 2) Respiratory infection preceded the onset of CVA in 3 subjects. 3) Cough was generally nocturnal, but 2 subjects coughed only in the daytime. 4) FEV1.0% was decreased (less than 70%) in only 2 subjects, whereas V25 was decreased (less than 80% of predicted value) in 11 out of 12 evaluable subjects, which suggested peripheral airway obstruction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical study on cough variant asthma]. 150 83

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congestive heart failure in elderly readmitted patients]. 152 7

Serum angiotensin converting enzyme (ACE) activity was determined in 46 children with congenital heart disease with normal and abnormal lung perfusion: (1) congenital heart disease with normal pulmonary blood flow (12 patients); (2) congenital heart disease with increased pulmonary blood flow (18 patients); (3) congenital heart disease with decreased pulmonary blood flow (16 patients). There was no significant difference in serum ACE activity between the three groups. In group 2 serum ACE activity had a tendency to correlate inversely with both mean pulmonary arterial pressure (r = -0.43; P less than or equal to 0.05) and pulmonary vascular resistance (r = -0.48; P = 0.05). No further correlations between serum ACE activity and age, serum electrolytes, creatinine nor other haemodynamic data could be established.
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PMID:Angiotensin converting enzyme activity in children with congenital heart disease. 196 19

Coronary heart diseases are three times more common in hypertensives older than 65 than in normotensive patients with comparable risk profiles. To be effective, cardioprotection must cover both elevated blood pressure and its consequences for the myocardium and coronary vessels (myocardial hypertrophy, microangiopathy and macroangiopathy), and should employ substances that have an effect on the underlying pathophysiological processes of hypertension and hypertensive cardiopathy. These preconditions are, at least in part, met by calcium antagonists, ACE-inhibitors and beta blockers. They have been proved to bring about a lasting decrease in blood pressure, and regression of cardiac enlargement. Regression of coronary sclerotic changes, however, is not yet certain. Overadditive effects have been described for the combination of calcium antagonists and ACE-inhibitors.
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PMID:[Medicamentous cardioprotection. 2: Hypertension]. 213 95

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)
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PMID:Major new developments affecting treatment and prognosis in hypertension. 235 5

The paper deals with causes of arterial hypertension in the early postperfusion and postoperative periods in treating congenital heart disease (CHD) under artificial circulation (AC). The hemodynamics and parameters of the renin-angiotensin-aldosterone system (RAAS) were examined clinically and biochemically in 100 patients. The findings showed that under hypothermic perfusion with nonpulsing blood flow, plasma renin activator and angiotensin converting enzyme became activated to affect the dynamics of mean arterial blood pressure. A method for RAAS blockage under AC has been developed, which includes administration of sodium thiopental and baralgin during AC. The method provides for reliable prevention of RAAS components activation and guarantees the normalization of the mean arterial pressure in the postperfusion and early postoperative periods.
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PMID:[Arterial hypertension of unclear etiology as a complication of anesthesia during heart surgery under conditions of artificial circulation]. 235 29

It seems established that hypertension, to some degree, is a frequent consequence of cardiac transplantation. The hypertension occurs de novo and is not related to whether hypertension was present in association with the heart disease that led to the need for transplantation. The etiology of this hypertension is multifactorial and varies depending on the time that has ensued after transplantation. Acutely, it is primarily a problem related to intravascular volume expansion and persistently increased systemic vascular resistance. Although it may be modest in severity, it seems to be particularly resistant to therapy with most antihypertensive drugs. Moreover, the total "hyperbaric impact" of the hypertension is rendered greater because the blood pressure and heart rate in these patients with denervated hearts fails to show the usual 10 to 15 percent fall when recumbent/asleep at night, which occurs in normotensive individuals and in most with hypertension of other etiologies. The major factor in the persistence of the hypertension through the later stages post-transplantation appears to be the cyclosporine that is used as an immunosuppressive. Although cyclosporine has been the major contributor to reduced rejection in these individuals, and to their increasingly prolonged survival, it inevitably produces slowly progressive impairment of renal function. The damage to the kidney is reflected both in tubular as well as glomerular and vascular damage, with a steady fall in glomerular filtration and a rise in creatinine. From our studies it appears that the renal alterations are associated with a gradual rise in plasma renin activity and angiotensin II, which perhaps further damages the kidney and causes persistence of the increased systemic vascular resistance. The use of lower doses of cyclosporine during the ischemic phase in the kidney that immediately follows surgery and of reduced doses over time, often with azathioprine added, seems to minimize the renal damage, or at least to stabilize it and to slow progression of the renal dysfunction and hypertension. Treatment of the hypertension with conventional drugs has definite but limited value. Diuretics and vasodilators have been the mainstay of our approach during the early phases of the hypertension but our recent data indicate that ACE inhibitors may become relatively specific in management during the later phases of the post-transplantation period as PRA levels rise in response to vascular damage by cyclosporine. ACE inhibitors have inherent dangers that require careful monitoring.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertension following orthotopic cardiac transplantation. 240 98

The anti-anginal effect of the ACE inhibitor enalapril, at a dosage of 5 mg twice a day, was tested in a randomised, placebo-controlled double-blind trial on 12 normotensive patients with proven coronary-heart disease. There was a reduction of exercise-induced ST depression by 22% already after the first dose of 5 mg. After 15 days of treatment the ST depression had decreased by 35% (P less than 0.05).
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PMID:[Anti-ischemia effect of enalapril in coronary heart disease. A randomized placebo-controlled double-blind study]. 283 91

Plasma levels of atrial natriuretic peptide (ANP) were measured in patients with organic heart disease undergoing diagnostic cardiac catheterization. Independent of nature and duration of the disease (valvular heart disease, congestive cardiomyopathy) plasma ANP levels were closely related to the severity of cardiac failure. Furthermore, plasma ANP levels were found to be negatively correlated with the cardiac index and to be positively correlated with right and/or left atrial and with pulmonary artery pressures. During physical exercise (bicycle ergometer) a marked increase of plasma ANP levels was observed, which was closely related to increments in mean pulmonary artery pressure. This rise in plasma ANP levels during physical exercise was not attenuated in patients with already elevated resting plasma concentrations of ANP. In patients with congestive cardiomyopathy, afterload-reduction by ACE-inhibition resulted in changes of central hemodynamics, which were closely reflected by venous concentrations of ANP. The measurement of plasma ANP levels may serve as an indicator of the severity of cardiac failure. Plasma concentrations of ANP, however, are neither helpful in establishing the etiology of the underlying heart disease nor in differentiating left and right heart failure. However, in cases of already established organic heart disease plasma ANP levels may be used as a marker for assessing the efficacy of the therapeutic regimen.
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PMID:[Does the measurement of plasma ANP have a diagnostic or prognostic value in patients with organic heart disease?]. 297 Jan 74

Inhibition of the angiotensin converting enzyme (ACE) is associated with a decrease in renal vascular resistance, an increase in renal blood flow and a redistribution of intrarenal blood flow toward juxtamedullary nephrons. In general, ACE-inhibition does not affect normal glomerular filtration rate (GFR) but may increase GFR in patients on a low sodium intake prior to treatment. Since the rise in GFR is smaller than the rise in renal blood flow, in most instances a decrease in filtration fraction will result. In contrast to other vasodilator drugs, the decrease in blood pressure induced by ACE-inhibition is not accompanied by sodium retention, but rather by an initial natriuresis. ACE-inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. The initial positive potassium balance after ACE-inhibition may protect patients with heart disease from potentially hazardous arrhythmias. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydrosmotic effect of vasopressin and thus result in a rise in free-water clearance. Finally, based on experimental evidence, long-term treatment with ACE-inhibitors may have a protective effect on renal function by reducing glomerular filtration pressure.
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PMID:[Inhibition of the angiotensin-converting enzyme--effect on kidney function and electrolyte balance]. 306 59


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