Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with congestive heart failure (CHF) due to dilated cardiomyopathy, nifedipine, diltiazem and several of the newer calcium antagonists including nicardipine, nitrendipine, felodipine and PN 200-110 (isradipine) improve left ventricular function. Because of its relatively more pronounced negative inotropic and chronotropic actions, verapamil is generally not tolerated by patients with left ventricular failure. In addition, even relatively vascular-selective agents such as nifedipine can occasionally cause significant left ventricular depression, particularly if combined with beta-adrenergic blocking agents. Comparative studies using nitroprusside to cause an equivalent decrease in arterial pressure indicate that nifedipine acts predominantly on the arterial vasculature, and that a small but significant decrease in contractility occurs, apparently due to a direct myocardial action. Although diltiazem causes a depression in myocardial contractility in dogs with volume overload heart failure, limited data show no significant negative inotropic action in patients with heart failure. The negative inotropic effects, if any, of newer and possibly more vascular-selective agents are not yet known. Calcium antagonists appear to act predominantly on the limb and coronary vasculature, with relatively less effect on renal and hepatic vessels. In patients with CHF, nifedipine causes an increase in coronary blood flow and a decrease in the aorto-coronary sinus oxygen difference indicating an improvement in myocardial energetics. Although nifedipine causes an increase in cardiac index and decreases in systemic vascular resistance and pulmonary capillary wedge pressure during exercise, the limited data available fail to show a short- or long-term increase in exercise capacity. Nifedipine causes an increase in plasma renin activity, possibly due to a direct action on the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Usefulness of calcium antagonists for congestive heart failure. 354 90

From June 1977 to February 1986 we studied 31 children with dilated cardiomyopathy. Seven patients (22%) aged 8 months to 3 years had associated congenital cardiac lesions--tetralogy of Fallot (3), coarctation of the aorta (2), ventricular septal defect (1) and Ebstein's malformation (1). The diagnosis was confirmed by hemodynamic and angiographic studies in 5 patients and by autopsy in 2. Although different congenital lesions were present, all 7 patients had congestive heart failure, flattening of T-waves or ST-segment depression on the electrocardiogram and significant decrease in the left ventricular shortening fraction as judged by echo. We conclude that the incidence of dilated cardiomyopathy associated with congenital heart malformations is high in our pediatric population. The clinical status of patients appears to be more dependent on the improvement of dilated cardiomyopathy and less dependent upon the underlying congenital heart malformations.
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PMID:Congenital heart malformations associated with dilated cardiomyopathy. 366

The treadmill exercise test with the Bruce protocol was performed in three patients with post-myocarditic myocardial hypertrophy (PMH) and ten patients with cardiomyopathy, including three with dilated cardiomyopathy (DCM), five with hypertrophic obstructive cardiomyopathy (HOCM), and two with hypertrophic and nonobstructive cardiomyopathy (HCM). The endurance time was below the normal level in all but one case and was normal or near normal in the three cases with PMH. ST depression was observed in five cases, none of which were of HCM. A marked increase in amplitude of the negative phase of the P wave in V1 was observed in one patient with DCM. The response of blood pressure during the exercise was abnormal in patients with DCM and HCM but was normal in PMH.
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PMID:Treadmill exercise test in children with cardiomyopathy and postmyocarditic myocardial hypertrophy. 372 84

A congestive cardiomyopathy (CCM) model occurs in inbred broad-breasted turkeys and is manifested by reduced hatchability and a high mortality within a week of hatching. In the survivors, cardiac dilation begins by 3-4 weeks of age and further mortality occurs from chronic congestive heart failure. The mechanisms behind these changes is unknown, and, therefore, we investigated what role, if any, myocardial energy metabolism might play in these events. Ventricular myocardial samples were obtained for analysis of adenine nucleotides (ATP, ADP, AMP) and creatine phosphate (CP) in control and CCM turkeys, 1-31 days old. The adenine nucleotide energy charge (EC) was calculated using the formula EC = ATP + 1/2ADP/(ATP + ADP + AMP). We found the myocardial ATP levels and EC in CCM hearts at 1-2 days were reduced. In control turkeys, no significant age-related differences were found in myocardial high-energy phosphate compounds or in the EC. This depression in the energy metabolism of CCM turkeys may also be reflected in their poor hatchability. By 6-10 days, however, ATP levels had recovered and remained normal despite the onset of cardiac dilation and failure at 3-4 weeks of age in CCM turkeys. Because CP levels in control and CCM turkey hearts were similar in all age groups, significant ischemia did not appear to be present after hatching in CCM turkeys. Our results suggest, therefore, that an insult probably prior to hatching produced depressed myocardial energy levels in CCM turkeys and led to reduced hatchability. This early insult appears to be significant, in that late cardiac dysfunction resulted despite the recovery of myocardial ATP levels.
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PMID:Myocardial high-energy phosphate levels in cardiomyopathic turkeys. 376 30

A study was made of the functional activity of natural killer cells (NK-cells), antibody dependent cellular cytotoxicity of killer cells (K-cells) and the effect of interferon (alpha-IFN) in vitro on function of these cells in a group of donors and patients with dilated cardiomyopathy (DCMP) as well as in patients with chronic coronary heart disease (CHD) and myocardial infarction (MI). Patients with DCMP might be divided into 3 groups according to the nature of NK- and K-cell functional activity: in a grave and rapid DCMP course the functional activity of NK- and K-cells was sharply decreased, a favorable course of disease was characterized by normal or raised values of their cytotoxicity. Patients with a severe type of DCMP revealed profound depression of lymphocyte killer activity.
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PMID:[Antibody-dependent and natural cellular cytotoxicity in patients with dilated cardiomyopathy]. 379 51

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
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PMID:Cardiac Wilson's disease. 382 52

Aortic input impedance and hydraulic power were derived from simultaneous catheter recordings of ascending aortic pressure and velocity in eight normal subjects and 11 age-matched subjects with clinical heart failure secondary to idiopathic congestive cardiomyopathy. Resting data revealed the characteristic depression of cardiac output and elevation of systemic vascular resistance in patients with heart failure. The pulsatile component of vascular hydraulic load, characteristic impedance (Zc), was similar in both groups (Zc normal: 85 +/- 30 dyne-sec-cm-5; Zc cardiomyopathy: 93 +/- 33 dyne-sec-cm-5). The oscillatory fraction of aortic input power in patients with heart failure (14 +/- 4%) was also similar to that of normal subjects (11 +/- 2%). The transition from rest to exercise in patients with heart failure was marked by a decrease in the steady component of arterial hydraulic load, although characteristic impedance did not change. A similar qualitative response occurred in normal subjects, although the systemic vascular resistance during exercise remained above normal in patients with heart failure. The modulus of the first harmonic of impedance significantly decreased during exercise in normal subjects but did not change significantly in patients with heart failure. Furthermore, the modulus of the first harmonic of the reflection coefficient decreased significantly during exercise in normal subjects but did not change in patients with heart failure in spite of systemic vasodilation. Exercise appears to impose no additional increase in vascular hydraulic load on the ejecting left ventricle. The similar aortic characteristic impedances in patients with heart failure and in normal subjects, at rest and during exercise, are consistent with a constant oscillatory fraction of input power.
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PMID:Characteristics of vascular hydraulic load in patients with heart failure. 400 37

Left ventricular (LV) diastolic properties in dilated cardiomyopathy (DCM), transmural myocardial infarction (TMI), and hypertrophic cardiomyopathy (HCM) were evaluated. Radionuclide angiography and M-mode echocardiography were performed for 11 cases of DCM, 40 cases of TMI, 21 cases of HCM, and nine normal control subjects. In DCM, the peak filling rate (PFR) and filling fraction (FF) were significantly reduced, but the time to the peak filling rate (TPFR) was not prolonged. In TMI, both the PFR and FF were significantly reduced. Moreover, the TPFR was significantly prolonged in TMI as compared to DCM. Although depression of the PFR in HCM was not apparent, prolongation of the TPFR in HCM was marked. In DCM, there was good correlation between the PFR and left ventricular ejection fraction (EF) (r = 0.71, p less than 0.03). In TMI, there was a good correlation between the TPFR and the standard deviation of the LV phase angle histogram (SDP), indicating LV asynergy (r = 0.589, p less than 0.005). In HCM, both the FF and PFR correlated inversely with the LV wall thickness (r = -0.74, p less than 0.008; r = -0.581, p less than 0.03, respectively). These results indicate that various factors affect LV diastolic properties in heart disease, and that radionuclide angiography is a valuable technique for evaluating LV diastolic function.
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PMID:[Left ventricular diastolic properties in dilated cardiomyopathy, transmural myocardial infarction, and hypertrophic cardiomyopathy]. 406 40

It is known that the heart will adapt to actual demand by increasing or decreasing its size through different mechanisms. In this presentation, the possible role of catecholamines in regulating heart protein synthesis and developing cardiac hypertrophy and cardiomyopathy is discussed. Injecting animals with catecholamines has been found to induce cardiac hypertrophy. In vitro perfusion of rat heart in the presence of catecholamines has been found to induce a time-dependent and dose-dependent stimulation of amino acid transport and incorporation into proteins. Acute haemodynamic effects of catecholamines increase cardiac performance while long-term treatment seems to cause depression of cardiac function, especially during ischaemic conditions. Chronic beta-blockade in patients with primary congestive cardiomyopathy improved both cardiac function and clinical condition in more than half the patients. Furthermore, a beneficial effect on survival was also found, when compared with a matched control group. It is hypothesised that catecholamines may play a role in developing cardiac hypertrophy as well as congestive cardiomyopathy.
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PMID:Possible adrenergic effects on heart protein metabolism. 613 40

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


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