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

Patients with paroxysmal atrial fibrillation (PAF) are prone to recurrence. We compared the efficacy and tolerability of flecainide acetate in the control of PAF by means of conventional treatment with quinidine in 19 patients without structural heart disease. A randomized, placebo-controlled, crossover protocol consisting of 8 weeks of treatment with either agent was used. The recurrence of PAF was documented in a symptom diary and confirmed by event ECG recording. Complete control of symptoms was achieved in 4 of 19 and 2 of 11 of patients with flecainide and quinidine, respectively. Both agents prolonged the time to the first recurrence and significantly reduced the total duration of PAF recurrence by 40% and 47%, respectively (p less than 0.05 compared with placebo). Compared with quinidine, flecainide significantly reduced the frequency of recurrence and the rate of PAF during a recurrent episode. However, treatment with flecainide was associated with a higher incidence of symptomatic sinus pauses and visual disturbances compared with a higher incidence of gastrointestinal side effects with quinidine. During a follow-up period of 32 months, satisfactory control was achieved in 74% of patients with the use of these two antiarrhythmic agents.
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PMID:A randomized double-blind crossover study comparing the efficacy and tolerability of flecainide and quinidine in the control of patients with symptomatic paroxysmal atrial fibrillation. 151 92

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

The forms of administration, mechanisms of action, side effects and complications, and other aspects of female hormonal contraception are set forth in this "lesson" for medical students. Female hormonal contraception has been in use for over 30 years and is used by more than 150 million women worldwide. Oral contraceptives suppress the preovulatory peak of follicle stimulating hormone and luteinizing hormone, preventing ovulation and follicular maturation. Progestins render the cervical mucus impermeable to sperm and modify the endometrium so that it will no longer support implantation. The synthetic estrogen ethinyl estradiol is used in most combined oral contraceptives (OCs). Among the numerous progestins in use are the newer desogestrel, gestodene, and norgestimate, which have fewer androgenic and metabolic effects than did the 1st generation. the different forms of administration of hormonal methods include combined OCs, oral preparations containing low doses of progestin continuously administered or high doses continuously or discontinuously administered. Intramuscular injection of progestins and the so-called "morning after" postcoital pills are less often prescribed. The combined preparations may be monophasic, biphasic, triphasic, or sequential. Sequential preparations should be avoided because of the hyperestrogenic climate they induce. The low-dose progestin preparations are indicated for women with contraindications to synthetic estrogen. They must be taken at the same time each day and have a relatively high rate of side effects, especially ovarian and breast cysts and irregular bleeding. High-dose progestin preparations have significant metabolic effects and are indicated primarily for patients with gynecological problems such as fibromas and endometriosis. Intramuscular injection of medroxyprogesterone acetate every 3 months is effective but has the same side effects as high-dose progestins. It is indicated primarily for patients unable to control their own behavior. The hormonal methods are all highly effective in preventing pregnancy when correctly administered. Side effects may be minor problems, such as nervousness and nausea, that are usually of short duration. the more serious side effects, including modifications of lipid or carbohydrate metabolism, hemostasis, blood pressure, or hepatic functioning and cardiovascular effects, have been reduced with the new lower dosed formulations. Absolute contraindications to hormonal contraception include undiagnosed vaginal bleeding or amenorrhea, history of thromboembolic or cerebral vascular accidents, severe cardiopathy or hypertension, hyperlipidemia, hepatopathy, hormonodependent cancer, pituitary tumors, porphyria, and severe mental problems. Relative contraindications impose the need for careful monitoring and follow-up. The practitioner should be aware of the possibility of interactions between OCs and certain other drugs.
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PMID:[Hormonal contraception]. 160 74

Immunoglobulin abnormalities in serum from 76 heart-transplant recipients were examined by cellulose acetate and agarose gel electrophoresis. Monoclonal components were typed by immunofixation. IgG, IgA, and IgM and total kappa and lambda light chains were quantified by immunonephelometry. We confirm that both monoclonal and oligoclonal immunoglobulin banding are common in serum from these patients. Of the 149 serum samples examined, 21 (15%) had one monoclonal component and 53 (35%) had two or more. These monoclonal immunoglobulins were generally present at a low concentration and were transient. The class of immunoglobulins most commonly involved was IgG (about sevenfold more numerous than IgM); monoclonal IgA components and free light chains were not detected. The nephelometric kappa/lambda and heavy chain/light chain ratios were poor indicators of these abnormalities. Immunoglobulin abnormalities were not correlated with the sex and age of recipients, the pre-existing cardiopathy, the time since transplantation, or plasma concentrations of cyclosporine, but did correlate with plasma immunoglobulin concentration, biopsy findings, and viral infections, especially cytomegalovirus (CMV). A monoclonal IgG purified from a patient with a high titer of anti-CMV antibodies did not react with CMV antigens. The origin of these immunoglobulin abnormalities is unclear. Our data suggest that the presence of monoclonal or oligoclonal banding in heart-transplant recipients is of limited prognostic significance.
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PMID:Monoclonal and oligoclonal gammopathies in heart-transplant recipients. 173 99

Eosinophilic endocarditis is a potentially lethal complication of chronic peripheral blood hypereosinophilia. We hypothesized that eosinophil peroxidase (EPO), an abundant eosinophil (EO) cationic granule protein, promotes eosinophilic endocarditis by binding to negatively charged endocardium, and there generating cytotoxic oxidants. Using an immunocytochemical technique, we demonstrated endocardial deposition of EPO in the heart of a patient with hypereosinophilic heart disease. Because EPO preferentially oxidizes Br- to hypobromous acid (HOBr) rather than Cl- to hypochlorous acid (HOCl) at physiologic halide concentrations, we characterized the Br(-)-dependent toxicity of both activated EOs and purified human EPO towards several types of endothelial cells and isolated working rat hearts. In RPMI supplemented with 100 microM Br-, phorbol myristate acetate-activated EOs, but not polymorphonuclear leukocytes, caused 1.8-3.6 times as much 51Cr release from four types of endothelial cell monolayers as in RPMI alone. H2O2 and purified human EPO, especially when bound to cell surfaces, mediated extraordinarily potent, completely Br(-)-dependent cytolysis of endothelial cells that was reversed by peroxidase inhibitors, HOBr scavengers, and competitive substrates. We further modeled eosinophilic endocarditis by instilling EPO into the left ventricles of isolated rat hearts, flushing unbound EPO, then perfusing them with a buffer containing 100 microM Br- and 1 microM H2O2. Acute congestive heart failure (evidenced by a precipitous decrement in rate pressure product, stroke volume work, aortic output, and MVO2 to 0-33% of control values) ensued over 20 min, which deletion of EPO, Br-, or H2O2 completely abrogated. These findings raise the possibility that EPO bound to endocardial cells might utilize H2O2 generated either by overlying phagocytes or endogenous cardiac metabolism along with the virtually inexhaustible supply of Br- from flowing blood to fuel HOBr-mediated cell damage. By this mechanism, EPO may play an important role in the pathogenesis of eosinophilic endocarditis.
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PMID:Bromide-dependent toxicity of eosinophil peroxidase for endothelium and isolated working rat hearts: a model for eosinophilic endocarditis. 198 18

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

The cardiovascular effects of oral contraceptives, as predicted by studies on serum lipid changes in users, are based on the progestin dose, androgenic potency and biologic effect of the estrogen in the pill. Women suffer 250,000 deaths per year in the U.S. resulting from cardiovascular disease, almost half as many as men. They have the same risk factors: high cholesterol, high blood pressure and smoking, and also have more risk from diabetes than men do. The serum HDL, especially HDL2, correlates closely and inversely with heart disease risk. Exogenous estrogens raise HDL and HDL2, and lower LDL, conferring protection against coronary disease, in direct proportion to dose. Progestins usually have adverse effects, in proportion to dose, but progestin potency and type also determine their effects. The estrane progestins norethindrone, norethindrone acetate and ethynodiol diacetate are less potent and much less androgenic, while the gonanes norgestrel and especially levonorgestrel are 5-20 times as potent and androgenic. Each pill needs to be considered as a unit. Several comparative studies are reviewed, corroborating the prediction that pills with higher progestin potency have adverse effects on serum lipids, compared to those with higher estrogen effect. For new lower dose multiphasics, the effects either way are minimal, but HDL2 is still significantly lowered by pills containing levonorgestrel. Progestin-only pills lower HDL2 17- 21%. It is prudent to follow and treat the long-term effects of oral contraceptives on blood lipids.
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PMID:Oral contraceptives and cardiovascular risk. Taking a safe course of action. 220 2

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

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


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