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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of nifedipine and nitroglycerin on the diameter of epicardial coronary arteries, the stenosis diameter, as well as arterial blood pressure and heart rate were recorded in 20 patients with coronary-heart disease. Nifedipine (20 mg sublingually) caused a significant fall in arterial pressure and a significant rise in heart rate. Additional administration of nitroglycerin (0.8 mg sublingually) caused a further fall in arterial pressure while heart rate remained constant. A definite relaxation (vasodilatation) of the epicardial vessels was demonstrated after nifedipine and a further increase after nitroglycerin. While nifedipine on average led to a significant increase in the diameter at the site of stenosis, response of individual stenoses was highly variable. In one patient with subtotal stenosis of the anterior interventricular branch a complete, transitory occlusion at the site of the stenosis occurred during nifedipine medication. This paradoxical reaction was not noted after nitroglycerin. Relaxation of the epicardial coronary arteries by nifedipine with suppression of phasic tone thus seems to be the major part of its anti-anginal effect. This effect is potentiated by nitroglycerin so that the combination of nitrate and calcium-antagonist appears to be therapeutically reasonable. In individual patients, however, there may be a paradoxical reaction to nifedipine.
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PMID:[Effect of nifedipine and nitroglycerin on epicardial vessels in coronary heart disease]. 642 31

In a naturally occurring model of congestive cardiomyopathy-round heart disease of turkeys, Ca2+ transport of isolated cardiac sarcoplasmic reticulum was evaluated at 1, 10, 28, and 56 days of age. Ca2+ binding in round heart disease birds was reduced to between 55% and 75% of values measured in age-matched commercial control turkeys (P less than 0.05 to less than 0.01). Similarly, Ca2+ uptake in round heart disease birds was reduced to between 52% and 87% of values measured in age-matched commercial control turkeys (P less than 0.05 and less than 0.01). Ca2+-stimulated ATPase values were similar in 1-, 10-, and 28-day-old round heart disease and commercial control turkeys. However at 56 days of age, when all round heart disease birds showed moderate to marked left ventricular dilatation. Ca2+-stimulated ATPase was reduced to 75% of control values (P less than 0.05). Depression of Ca2+ binding and Ca2+ uptake preceded the appearance of cardiac dilatation and may contribute to the pathogenesis of round heart disease. Depression of Ca2+-stimulated ATPase, present only after cardiac dilatation developed, appears to be secondary to cardiac failure. Sarcoplasmic reticulum function in round heart disease birds immunosuppressed by cyclophosphamide treatment (40 mg . kg-1 . d-1 for the first 4 days of age) was evaluated at 10 days of age. This treatment increased Ca2+ binding by 73% (P less than 0.05), and Ca2+-uptake by 58% (P less than 0.01) over values measured in untreated round heart disease birds. Reversal of the altered Ca2+ transport in sarcoplasmic reticulum by early immunosuppression supports the hypothesis that the immune system plays an integral part in the development of the congestive cardiomyopathy of round heart disease.
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PMID:Early alterations in the function of sarcoplasmic reticulum in a naturally occurring model of congestive cardiomyopathy. 645 87

Calcium ions have been shown to be involved in smooth muscle contraction and various secretory processes. Nifedipine, a calcium channel blocking drug, does not have any intrinsic bronchodilatory effect, but it has been suggested to possibly inhibit bronchial reactivity. Eight patients, with normal baseline pulmonary function studies and methacholine-induced bronchial reactivity, had a repeat metacholine challenge after nifedipine. Spirometry was obtained at baseline and three minutes after successive inhalations of normal saline and five, 15, 30, 50, 100 and 200 inhalation units of 0.5% methacholine. Plethysmographic lung volumes and airways resistance were measured at the start of the test and after the last inhalation of methacholine. The FEV1, FVC, MMEF and PEFR were reduced by an average of 35.6%, 20.6%, 54.4% and 30.6%, respectively, on the initial study, and by 35.4%, 20.5%, 54.8% and 34.5% after nifedipine. Airways resistance was increased by 249.3% in the initial study and by 265.7% after nifedipine. There was no statistical difference in baseline spirometry, spirometry obtained at any level of methacholine inhalation, or in airways resistance between the two studies. Despite comparable decreases in lung function, all patients were less symptomatic after receiving nifedipine. Nifedipine does not alter methacholine-induced bronchial reactivity. Until the role of nifedipine in asthma is better defined, caution should be used in prescribing nifedipine to asthmatic patients with heart disease, because their perception of airways resistance may be altered.
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PMID:Nifedipine does not alter methacholine-induced bronchial reactivity. 650 50

To document the independent effects of acute changes in preload, afterload and inotropic state on the systolic time intervals, 10 isolated rat left ventricular muscle preparations were studied. Experiments were performed using physiologically sequenced contractions that simulate the loading conditions of the intact left ventricle. The preshortening period was measured from the time of the electrical stimulus to the onset of muscle shortening, and the isotonic contraction time was measured as the duration of shortening. These variables are analogous to the preejection period and the left ventricular ejection time in the intact heart. It was found that an isolated increase in preload shortened the preshortening period and prolonged the isotonic contraction time, whereas an increase in afterload prolonged the former and shortened the latter. Isoproterenol shortened both the preshortening period and the isotonic contraction time, while an increase in calcium shortened the preshortening period and lengthened the isotonic contraction time. All changes were significant (p less than 0.01) by analysis of variance. Thus, the similar dependence of preshortening period, isotonic contraction time and clinical systolic time intervals on changes in preload, afterload and inotropic state supports the derivation of systolic time intervals from fundamental principles of myocardial mechanics. These data provide an improved basis for the rational interpretation of systolic time intervals in patients with and without heart disease.
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PMID:Systolic time intervals: assessment by isolated cardiac muscle studies. 663 Jul 74

This report summarizes the spectrum of clinical and immunologic findings gathered prospectively in 13 patients with the DiGeorge syndrome. Our patients demonstrated marked variability in both the clinical manifestations and the degree of immunodeficiency, confirming the findings of earlier individual case reports and retrospective autopsy reviews. Ages at the time of presentation ranged from one day to 4 months. Congenital heart defects including truncus arteriosus, ventricular septal defect, interrupted aortic arch, and tetralogy of Fallot commonly brought these infants to medical attention within the first two weeks of life. Abnormal calcium homeostasis was found in all patients. Those patients presenting after the first month of life often had hypocalcemic seizures as the initial clinical manifestation. Parathyroid hormone levels and the number and location of parathyroid glands varied considerably. Immunologic evaluation revealed that total lymphocyte counts, percent T-cells, total T-cells, and T-lymphocyte function ranged from normal to severely depressed. The most consistent immunologic abnormality, found in 11 of the 13 patients, was a decrease in total T-cells. Sequential studies in five patients demonstrate that spontaneous resolution of immunodeficiency may occur in some, yet progressive loss of immune function may be observed in others. Complete immunologic evaluation and careful followup is mandatory in infants with persistent hypocalcemia and congenital heart disease who are suspected to have DiGeorge syndrome.
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PMID:Clinical and immunologic spectrum of the DiGeorge syndrome. 697 33

Nifedipine is a calcium antagonistic drug which reduces elevated vascular resistances. The hemodynamic effects of 20 mg of sublingual nifedipine were studied in 10 patients with chronic pulmonary hypertension. The etiology of pulmonary hypertension was chronic lung disease in 4, congenital heart disease in 2, mitral stenosis in 1, recurrent pulmonary embolism in 2 and primary pulmonary hypertension in one case. 30' after the drug administration there was a fall both of total pulmonary vascular resistance (from 992 +/- 586 to 648 +/- 428 d s cm-5, p less than 0.02) and of systemic vascular resistance (from 1416 +/- 868 to 896 +/- 440 d s cm-5 p less than 0.02) with an increase of systemic cardiac index from 3.2 +/- 1 to 4.5 +/- 2 l/min/m'2 (p less than 0.02). No significant change in systemic arterial oxygen saturation was noted, while pulmonary arterial oxygen saturation increased from 56 +/- 16 to 62 +/- 13% (p less than 0.01). These hemodynamic changes persisted for 120' when a significant fall of mean pulmonary arterial pressure was also noted (from 59 +/- 11 to 52 +/- 9 mm Hg, p less than 0.02). These data indicate that nifedipine may be useful to reduce pulmonary resistance in pulmonary hypertension. However this effect was less pronounced in patients with chronic lung disease compared to the other cases. It is suggested that the type of pulmonary arterial changes may determine the hemodynamic response. Nifedipine may be particularly indicated when vasoconstriction (as in primary pulmonary hypertension) is the main determinant of pulmonary hypertension.
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PMID:Hemodynamic effects of nifedipine in pulmonary hypertension. 716 46

The importance of metals in normal and pathologic cardiovascular function has been recognized. Significant derangements in myocardial Ca2+, Mg2+, and Cu2+ have been reported in ischemic heart injury. We studied 3 groups of hearts: 1) fifteen specimens obtained from patients who had no heart disease, 2) nine specimens from patients who had expired from cyanotic congenital heart disease, and 3) ten specimens from patients who had expired from acute rheumatic heart disease with carditis and severe heart failure. None of the patients had undergone cardiac surgery. Left ventricular lateral wall Mg2+, Ca2+, Cu2+, and Zn2+ contents were measured by atomic absorption spectrometry. The results showed a significant decrease in myocardial Mg2- (Group I 177.06 +/- 32.71; Group II 155.66 +/- 14.79; Group III 149.00 +/- 13.29, p less than 0.05 and p less than 0.01, respectively), and Cu2+ contents (Group I 3.22 +/- 0.37; Group II 2.94 +/- 0.22; Group III 2.56 +/- 0.32, p less than 0.02 and p less than 0.001, respectively), and a rise in myocardial Ca2+ content (Group I 36.06 +/- 10.72; Group II 43.22 +/- 7.01; Group III 46.30 +/- 4.85, p = not significant, and p less than 0.01, respectively). The myocardial Zn2+ content did not change significantly (Group I 26.53 +/- 3.99; Group II 26.00 +/- 4.15; Group III 26.40 +/- 3.53). The myocardial Mg2+/Ca2+ ratio was reduced markedly in both groups (Group I 5.328 +/- 1.879; Group II 3.685 +/- 0.735; Group III 3.135 +/- 0.291, p less than 0.001 for both Groups II and III vs Group I). The latter results correlated closely with the myocardial Mg2+/Ca2+ ratios reported in experimental models in peri-infarction zones. Thus, the myocardium of patients who had expired from cyanotic congenital heart disease and acute rheumatic carditis is jeopardized by ischemia, with metal contents similar to the border areas in myocardial infarction.
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PMID:Myocardial metal content in patients who expired from cyanotic congenital heart disease and acute rheumatic heart disease. 717 80

To define the prevalence, frequency and characteristics of premature ventricular complexes (PVCs) in adults free of recognizable heart disease, we performed 24-hour ambulatory electrocardiography on 101 subjects (51 men and 50 women, mean age 48.8 years) in whom physical examination, chest x-ray, ECG, echocardiogram, maximal exercise stress test, right- and left-heart catheterization and coronary arteriography were normal. Thirty-nine subjects had at least 1 PVC/24 hours, but only four had more than 100 PVCs/24 hours and fewer than five had more than five PVCs in any given hour. The probability of having at least 1 PVC/24 hours increased with age (chi square = 11.789, p = 0.019). The number of PVCs/24 hours was also positively associated with age (4 = 0.33, p = 0.001). These was no consistent relationship between the presence or number of PVCs/24 hours and sex, blood pressure, weight, height, body mass index, serum potassium or calcium, cholesterol and triglyceride, hemoglobin, the ingestion of coffee, tea or alcohol, and cigarette smoking. Four subjects had multiform PVCs, two of whom had early PVCs.
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PMID:Premature ventricular complexes in the absence of identifiable heart disease. 722 80

Calcification of aortic homografts used for reconstruction of the right ventricular outflow tract was studied in assess the frequency of occurrence, location, extent, speed of progression, and clinical and hemodynamic implications. Radiologic follow-up by means of penetrated posteroanterior and lateral radiograms ranged from 2 to 10 years in two groups of patients. Group 1 comprised 40 patients with cyanotic congenital heart disease in whom an aortic homograft was used to restore continuity between the right ventricle and pulmonary arteries. Results from this group were correlated with those from Group 2, which included 80 patients who had a homograft implanted as a substitute for their own pulmonary valve, which had been used as an autograft for replacing the diseased aortic or mitral valve. In Group 1, 92% of the grafts were calcified 6 months to 4 years after operation. Calcification was severe in two cases, moderate in 33, and mild in two. One of the grafts had to be removed in the tenth postoperative year for progressive obstruction. In Group 2, 27% showed signs of calcification, never before the second year after implantation. Calcium development was severe in two, moderate in 12, and mild in eight. Two obstructed homografts were removed. Aortic homograft calcification has been more common, developed earlier, and been more severe in patients operated upon for congenital lesions. The lower age, the peculiar metabolism, the distorted anatomy, and the development of pulmonary hypertension in this group may account for this fact. In 96% of the patients who were followed, calcification has not yet meant clinical disability or hemodynamic dysfunction. Use of "fresh," antibiotic-sterilized homografts has reduced the incidence of calcification in Group 2 and is expected to decrease its severity in all cases.
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PMID:Calcification of aortic homografts used for reconstruction of the right ventricular outflow tract. 743 88

Little attention has been given to the question whether clinical heart failure can be a manifestation of hypocalcemia. A patient with hypoparathyroidism and heart failure prompted us to analyse the reports on this subject. The conclusion was that if associated with an underlying myocardial disease, hypocalcemia may be a rare contributing factor to hear failure. Hypocalcemic heart failure without coexisting heart disease has been suggested as a cause of hypotension in two special situations in which a sudden fall of serum ionized calcium is induced: massive transfusions of citrated blood and rapid correction of uremic acidosis. In addition to hypocalcemia and heart failure, our patient had exceptional repolarization disturbances: rate-dependent variation of T wave amplitudes during sinus arrhythmia and unexpected prolongations of the Q-T interval with attacks of ventricular tachycardia.
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PMID:A case of hypocalcemia, heart failure and exceptional repolarization disturbances. 743 43


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