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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

Corwin is a new, long-acting beta 1-adrenergic partial agonist for oral and intravenous (i.v.) use. The effects of corwin were compared with those of dobutamine in acute ischemic left ventricular failure in dogs. Failure was produced by embolization of the left main coronary artery with 50 micron plastic microspheres. This induced severe depression in left ventricular function, as evidenced by a marked increase in left ventricular end-diastolic pressure, reduction in left ventricular dP/dtmax, and cardiac output. After 45 min was allowed for stabilization, the 27 dogs were randomly assigned to three groups: control (n = 9), dobutamine-treated (5-10 micrograms/kg/min i.v., n = 9), and corwin-treated (0.025-0.10 mg/kg i.v., n = 9). The doses of dobutamine and corwin were adjusted to give an increase in left ventricular dP/dtmax of 50%. Both drugs similarly increased cardiac output (p less than 0.01), lowered left ventricular end-diastolic pressure (p less than 0.01) and total peripheral vascular resistance (p less than 0.01), but did not affect the heart rate. Only dobutamine increased the mean arterial pressure (p less than 0.01). Both drugs also increased the arterial concentrations and myocardial uptake of fatty acids (p less than 0.05) but caused only a small and nonsignificant increase in myocardial oxygen consumption. Our findings indicate that the hemodynamic and metabolic profiles of corwin and dobutamine are similar, and both drugs should be of special value in the treatment of congestive heart failure. Since corwin can be given orally and has a longer duration of action, it is potentially useful in the long-term treatment of heart failure.
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PMID:Comparative effects of dobutamine and corwin, a beta 1-adrenergic partial agonist, in experimental left ventricular failure. 241 Jul 22

Electrocardiographic body surface mapping on admission to coronary care has been shown to predict prognosis in a previous study of 100 patients with inferior wall acute myocardial infarction (AMI). A further 98 patients with first inferior wall AMI were now studied by body surface mapping on admission to coronary care to confirm that both the spatial distribution or map pattern of ST-segment potentials and the precise measurement of the maxima and minima are of prognostic significance. Each ST-segment map was compared by correlation coefficient to the average map pattern of the 4 groups derived in a previous study and placed in the group with the highest correlation coefficient. Analysis of these groups against outcome confirmed that the group dominated by a large area of marked anterior ST depression was associated with a high rate of complications and a significantly lower survival free of coronary artery bypass grafting (p less than 0.01). Patients in this group had more extensive and severe coronary artery disease than patients in the other groups. Increasing values of maximal ST depression correlated with mortality and complication rates. The extent by which the magnitude of ST-segment depression exceeded the magnitude of ST-segment elevation correlated with mortality and incidence of left ventricular failure. The results confirm the findings of the original study. Body surface mapping is of prognostic significance in inferior wall AMI.
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PMID:Prognostic significance of ST potentials determined by body surface mapping in inferior wall acute myocardial infarction. 275 75

The effect of therapy on exercise performance during a 3-year follow-up after acute myocardial infarction (AMI) was evaluated in a double-blind randomized comparison between 154 patients given metoprolol (100 mg twice daily) and 147 patients given placebo. Exercise tests were performed 1.5, 6, 12, 24 and 36 months after AMI. Maximal accomplished workloads were similar in the 2 groups throughout follow-up. Maximal heart rate was significantly higher in the placebo-treated group throughout the study (p less than 0.001). At the 6-week test more patients in the placebo group terminated exercise due to angina pectoris (40 vs 25%, p less than 0.05) and showed exercise-induced ST-depressions (38 vs 27%, p = 0.05) compared with the metoprolol group. Exercise-induced ventricular arrhythmias were significantly more common in the placebo group during the initial 6 months. Death, another AMI or both were significantly reduced by metoprolol treatment in patients with exercise-induced ST depression greater than or equal to 1 mm at the 6-week test. In a multiple logistic regression analysis maximal accomplished workload at 6 weeks (p less than 0.026), male sex (relative risk [rr] = 3.57, p = 0.016), previous AMI (rr = 3.07, p = 0.001), therapy with placebo (rr = 2.14, p = 0.007) and left ventricular failure (rr = 2.04, p = 0.023) were shown to carry independent prognostic information as well as exercise-induced ST-depression (greater than or equal to 1 mm) in placebo-treated patients (rr = 2.70, p = 0.01).
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PMID:Influence of long-term metoprolol treatment on early and late exercise test performance after acute myocardial infarction. 327 81

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

A group of 123 consecutive patients with acute transmural inferior myocardial infarction were compared according to the presence or absence of precordial ST segment depression on admission to hospital. There was a significant increase in mean age, peak creatine kinase levels, and the incidence of left ventricular failure and high grade atrioventricular block in the group with precordial ST segment depression. There was also an increase in in-hospital mortality in this group but this difference was not significant. Despite these differences in in-hospital progress, during a follow-up period of over two years there was no difference in long term mortality, recurrence of angina, or subsequent cardiac-related admissions between the two groups.
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PMID:Long term follow-up of inferior myocardial infarction. Prognostic significance of precordial ST segment depression. 386 34

The cardiopulmonary effects of continuous positive airway pressure (CPAP) were studied in 14 patients with acute myocardial infarction complicated by circulatory and respiratory failure. Cardiac performance, lung mechanics, and gas exchange were assessed during 50 percent mechanical ventilatory support at end-expiratory airway pressure levels of 0, 5, 10, and 15 mm Hg. The increase in airway pressure resulted in significantly improved arterial blood oxygenation (p less than 0.001) and in a substantial reduction in the spontaneous respiratory effort (p less than 0.001). We observed a slight decrease in stroke volume index (p less than 0.05) with increasing airway pressure in patients who had moderate left ventricular dysfunction, and a trend of improvement (NS) in those who had severe pump failure. Relatively high levels of CPAP can be used to improve pulmonary function in patients with acute myocardial infarction and left ventricular failure. In fact, circulatory depression is less likely to occur when cardiac performance is poor.
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PMID:Acute myocardial infarction complicated by left ventricular dysfunction and respiratory failure. The effects of continuous positive airway pressure. 388 Dec 27

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Apropos of 39 cases]. 391 82

In order to verify the usefulness of long-term digitalis therapy during physical rehabilitation in patients with recent myocardial infarction (MI) and left ventricular disfunction during exercise, 24 consecutive pts with PAedP greater than or equal to 25 mmHg (Swan-Ganz cath.) at maximal work load were selected. Pts with angina, ST depression (greater than or equal to 2 mm), complex ventricular arrhythmias (Lown 4-5), symptoms of left ventricular failure were excluded. At random 12 pts were assigned to group A (digoxin therapy) and 12 to group B (no therapy). Serum digoxin level was on average 1.48 ng/ml (range 1-2.85 ng/ml). Both groups performed over 4 weeks the same controlled training program. Before and soon after the end of the training period all pts underwent to an exercise test, standard chest x-ray films, 24 hour ambulatory ECG and two-dimensional echocardiography. No complication was observed during exercise test and training period. Age, myocardial infarction location, cardiac volume and hemodynamic behaviour during the first exercise test were similar in both groups. After training, maximal work capacity was increased in group A by 14% and in group B by 16% without significant changes in PAedP and Cl; at the same work load PAedP was lower in group B (-12%, p less than .02) while LVSWI was increased in both groups (14% and 17% respectively, p less than .05). No significant changes in cardiac volume, left ventricular asynergy, EF, and ventricular premature beats were observed. QT interval at rest decreased significantly only in group A 408 +/- 31 msec vs 371 +/- 34 msec (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recent myocardial infarction: role of digitalis therapy in patients with left ventricular dysfunction during exercise who participated in a short-term physical training program]. 400 49

Controversy exists over the nature of the abnormality in cardiac sympathetic nerves in heart failure. In the cardiomyopathy of the Syrian hamster, reduction in tissue stores and increased turnover of norepinephrine is clearly associated with excessive sympathetic stimulation but in animal models and humans with heart failure secondary to mechanical overload there is evidence for depression of neuronal uptake. Because norepinephrine is both released and taken up by sympathetic fibers it is impossible to assess norepinephrine kinetics in an intact heart without separating these two functions. A technique for doing so has recently been developed in normal dogs and we therefore acquired similar data in humans with heart failure secondary to chronic pressure and volume overload. The technique involves the combination of transient norepinephrine tracer coronary sinus outflow in relation to intravascular and interstitial references after simultaneous injection into the left coronary artery and the measurement of endogenous norepinephrine concentrations in artery and coronary sinus. We found a marked reduction in cardiac norepinephrine release and uptake in a group of patients with clinical left ventricular failure secondary to mechanical overload, relative to a group of patients with no failure. Norepinephrine balance and overflow across the heart were not significantly different. We conclude that there is hypofunction of the cardiac sympathetic nerves in heart failure secondary to mechanical overload and that traditional methods are inadequate in assessing cardiac norepinephrine kinetics when there are simultaneous changes in neuronal uptake and release.
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PMID:Tracer norepinephrine kinetics in coronary circulation of patients with heart failure secondary to chronic pressure and volume overload. 405 51


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