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)

Seventeen hypertensive patients with EKG evidence of left ventricular hypertrophy and subendocardial ischemia were studied. The following tests were performed: cine-ventriculography, coronary arteriography, ejection fraction, ventricular pressures, left ventricular mass, EKG stress test and atrial stimulation. In 10 cases cardiac scintigraphy with intracoronary injection of albumin-macro-aggregates marked with TC 99m, was obtained. EKG stress and atrial stimulation tests were positive in all cases, with ST depression greater than 1mm, or accentuation of previous ST depression. 83.7% of the patients had permeable coronary arteries, with "corkscrew' tortuosity. Left ventricular mass was increased in all cases (119 +/- 28.5% m2 s/c). Ejection fraction (74.2 +/- 8.1), and left ventricular diastolic pressures were normal. Cardiac scintigraphy showed uniform distribution of the radioisotope in the right ventricle and poor concentration with better dispersion and distribution in the left ventricle. It is concluded that subendocardial ischemia in these subjects is not produced by obstruction of the main coronary trunks and is associated to a significant increment of left ventricular mass which possibly produce a poor coronary reserve, and a potentially high risk condition.
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PMID:[Myocardial ischemia in hypertension heart disease (author's transl)]. 621 25

Since the early trials of antihypertensive drug treatment, regression of electrocardiographic evidence of left ventricular hypertrophy has been demonstrated. The first multiclinic trial in which these effects were reported was the Veterans Administration trial. In this study the development of abnormal QRS voltage, S-T segment depression or T-wave flattening or inversion in the treated patients was only one-fourth that found in the control group. In those patients with electrocardiographic evidence of left ventricular hypertrophy prior to randomization, reversal of the abnormalities occurred two and a half times more frequently in the treated patients then in the control patients. Other controlled trials have shown similar results with antihypertensive treatment. It is concluded that following antihypertensive drug treatment the electrocardiographic evidence of left ventricular hypertrophy in hypertensive patients is markedly reduced. However, the electrocardiographic signs associated with coronary heart disease did not seem to be altered.
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PMID:Electrocardiographic changes in the course of antihypertensive treatment. 622 87

The hemodynamic and contractile effects of acute cigarette smoking were analyzed in 35 patients with normal cardiac and coronary function as well as with cardiac failure and with coronary artery disease. In normal patients (normal ventricular function, normal coronary arteriogram) cigarette smoking exhibited no contractile depressant effects. Moderate increase in global and in regional wall motion and contractility was found. Likewise, in patients with compensated hypertensive hypertrophy (normal ventriculogram, significant left ventricular hypertrophy, normal coronary arteriogram) cigarette smoking increased global and regional contraction function. In cardiac disease patients (dilatative cardiomyopathy, advanced coronary artery disease, decompensated hypertensive heart disease) cigarette smoking was associated with depression in the overall and regional contraction behavior of the left ventricular myocardium. In patients with coronary artery disease, cigarette smoking was accompanied by marked depression of the regional contraction pattern in hypokinetic, akinetic, and dyskinetic zones. Moreover, contractile depression also occurred in the non-ischemic zones, without pre-existing coronary artery stenoses. In conclusion, acute cigarette smoking may not cause contractile depressant effects in normal patients and patients with compensated hypertensive hypertrophy. However, in coronary patients, significant negative inotropic effects are present not only in the ischemic zones, but also in the non-ischemic myocardium.
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PMID:Global and regional wall motion and contractility of the left ventricle following cigarette smoking. 623 23

With the purpose to study the haemodynamic changes that occur with myocardial ischaemia induced by atrial pacing (AP) in hypertensive heart disease, we studied 7 patients with such condition, all of them with a long time history of systemic hypertension, electrocardiographic signs at rest of left ventricular hypertrophy and ST-segment depression, at least of 0.5 mm. All the patients showed normal coronary arteries in angiocardiogram. AP was started 10 beats above the basal heart rate with increments of 10 beats every 2 minutes until a ST-segment depression at least of 2 mm was obtained which occurred in all the cases studied. After every 2 minutes of AP a simultaneous 12-leads electrocardiogram recording and left ventricular and aortic pull-back pressure were obtained. At the desired end point the AP was abruptly stopped and the same parameters were registered at 3, 5, 10 and 15 minutes until recovery. During AP the left ventricular systolic pressure (LVSP) did not show any significant change, with the exception of a patient who experienced angor pectoris during the proceeding. The left ventricular end-diastolic pressure (LVEDP) increased in 3.4 +/- 1.7 mmHg, change that was statistically significant (p less than or equal to 0.01) but not hemodynamically important since only in one patient it increased above the normal levels (from 13 mmHg basal to 17 mmHg during AP). In contrast, LVEDP markedly rose above normal when AP was stopped. It is concluded that neither LVEDP nor LVSP play an important role in the genesis of the ST segment depression seen in these patients. It is showed that, similar as in patients with obstructive coronariopathy, these cases work on a depressed Starling curve during AP and its recovery for what is thought that the functional meaning of ischaemia for both entities is similar no matter that their pathogenetic mechanisms are different.
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PMID:[Hemodynamic study in hypertensive cardiopathy under ischemia induced by atrial stimulation in the absence of fixed coronary obstructions]. 624 59

Congestive heart failure is associated with ventricular hypertrophy and dilatation, increased circulating catecholamines, and peripheral vasoconstriction. The extent to which these changes occur, whether they are a favorable "compensatory mechanism" or contribute to cardiocirculatory dysfunction, depends on the cause and severity of the heart failure. The addition of new sarcomeres through ventricular hypertrophy distributes the excess workload of the failing ventricle over more contractile units. In ventricular pressure overload, hypertrophy primarily increases wall thickness and ventricular volume is not usually increased; the converse is true with ventricular volume overload. Hypertrophy can result in enhanced or depressed contractile performance, depending on the stimulus for hypertrophy and method by which contractility is evaluated. The "ventricular function curve," which relates stroke volume to ventricular filling pressure or volume, overestimates the role played by the "Starling principle" as a compensatory mechanism and underestimates how well contractile performance is preserved. The evaluation of end systolic pressure-volume relationships under conditions of variable afterload closely reflects the isometric length-tension relationship and is therefore a more accurate way to quantitate cardiac muscle performance. Pressure overload hypertrophy usually leads to a depression in contractility whereas volume overload may not. An exaggerated sympathoadrenal response is another hallmark of severe heart failure that enhances contractility, helps initiate hypertrophy, and maintains arterial perfusion pressure. A generalized increase in peripheral vascular resistance occurs and is most prominent in those circulations most susceptible to neurohumoral control (renal, splanchnic, cutaneous). This favors perfusion of the cerebral and coronary circulations. Vasoconstriction is further enhanced by the activation of the renin-angiotensin-aldosterone system and secretion of ADH. This results in sodium retention and plasma volume expansion. In early mild heart failure, vasomotor tone may be normal at rest; however, the sympathoadrenal response to exercise may be intense. Moderate alpha receptor stimulation reduces skeletal muscle blood supply and favors the intramuscular redistribution of blood flow from inactive to active muscle fibers, thereby maintaining a normal oxygen consumption. During the later stages of heart failure, increased vascular stiffness due to increased sodium content and excessive norepinephrine appears to restrict nutritional blood flow to exercising muscle at the conductance-vessel level. Vasodilator drugs may reduce aortic impedance and improve cardiac output, may lower ventricular filling pressure, and relieve congestive symptoms, and may result in complex but favorable changes in the distribution of blood flow to the regional circulations.
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PMID:Cardiocirculatory dynamics in the normal and failing heart. 645 90

In routine reporting of electrocardiograms, a frequent problem is presented by the presence of repolarisation abnormalities (ST depression and/or T wave inversion) in the lateral leads without the accepted QRS voltage criterion of left ventricular hypertrophy. To help resolve this problem, the electrocardiograms of 41 patients with severe aortic stenosis who had no evidence of coronary disease were compared with the electrocardiograms of 20 patients with lateral myocardial infarction who had no clinical evidence of left ventricular hypertrophy. Nine of the patients with aortic stenosis were found to show repolarisation abnormalities in the lateral leads without the standard voltage criterion of left ventricular hypertrophy. The repolarisation pattern of aortic stenosis could frequently be distinguished from that of coronary disease by the presence of one or more of the following five features: depression of the J point, asymmetry of the T wave with rapid return to the baseline, terminal positivity of the T wave ("over-shoot"), T inversion in V6 greater than 3 mm, and T inversion greater in V6 than in V4.
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PMID:Electrocardiogram of pure left ventricular hypertrophy and its differentiation from lateral ischaemia. 645 13

The sample studied consisted of 46 patients with systemic hypertension. Of these, 21 had angor pectoris and constituted group I; 12 showed left ventricular hypertrophy, constituting group II; the other 13 subjects did not have complications and they formed group III. All patients, aside from the usual clinical evaluation, were submitted to exercise electrocardiography, coronary angiography and cineventriculography. The average age of patients in group III was lower than in the others (38.6 +/- 8.4 years), and so was the percentage of smokers (15.3%), and of patients with diabetes (23.0%). The number of smokers in group II represented 41.3% and in group I, 38%. The percentage of patients with diabetes was 33.3% in group II and 52.3% in group I. Pain in the patients of group I had the following characteristics: retrosternal pain was present in all cases, while referred pain to the neck and left arm appeared in 61% of the subjects. In 66.3% of the individuals the pain lasted between 5 and 15 minutes. In 52.3% of the group, pain was not always related to effort, but appeared also at rest. Temporal periodicity was present in 52.7% of the patients. Also in group I, 95.2% of the cases had a depression of the S-T segment in the leads corresponding to the anterior aspect of the left ventricle. In 86.6% of the subjects, there was a positive exercise test. The Sokoloff's index was 26.4 +/- 7.9 mm. In 75% of the subjects in group II, a depression of the S-T segment was present, and a positive exercise test was found in 50% of them. Their sokoloff's index was 26.7 +/- 6.4. None of the patients in group III had depressions of the S-T segment and 20% resulted with a positive exercise test. Their sokoloff's index was 13.3 +/- 2.9. The coronary angiography results showed stenosis in 28% of the subjects in group I and tortuosity of the vessels was apparent in 94.8% of them. None of the patients of group II and III had stenosis of the coronaries, but tortuosity was observed in 74.9% of the individuals in group II and in 69.1% of the cases in group III. Based in these data we conclude that there is a type of angor pectoris in hypertensive subjects which is related to hypertrophy of the left ventricle, but not to coronary stenosis. The management of this type of patient should be different to the regular one.
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PMID:[Clinical and coronary angiographic characteristics of hypertensive angina]. 645 72

To evaluate the clinical significance of ECG depolarization abnormalities of left ventricular hypertrophy, ECG findings were related to echocardiographic or autopsy left ventricular mass, geometry and function as well as hemodynamic overload, in a heterogeneous population of 161 patients. ST depression and asymmetric T wave inversion were present in 21/107 patients not receiving digitalis (19%) and in 33/54 (61%) receiving digitalis. In patients not receiving digitalis their prevalence increased linearly from 0% (0/31) with LV mass less than or equal to 100 grams to 100% (8/8) with LV mass over 400 grams (p less than 0.001). Patients taking digitalis manifested "strain" commonly despite a normal LV mass (4/14, 28%), but even more frequently with an LV mass over 200 grams (27/40, 68%) (p less than 0.05). In the absence of digitalis, repolarization abnormalities were also significantly associated with a reduced ejection fraction (8/17 or 47% versus 8/83 or 10%; p less than 0.001), increased LV internal diameter (9/18 or 50% versus 12/89 or 13%; p less than 0.01), and systolic blood pressure over 140 mm Hg (9/29 or 31% versus 7/61 or 11%; p less than 0.05). Increased thickness of the LV wall was not significantly associated with LV "strain" (p = 0.1). In this population, LV "strain" alone performed as well as other single or combined ECG criteria in the recognition of LVH (sensitivity 52%, specificity 95%). Thus, in the absence of digitalis, repolarization abnormalities are a highly useful ECG sign of LVH, despite numerous other factors capable of causing indistinguishable abnormalities.
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PMID:Repolarization abnormalities of left ventricular hypertrophy. Clinical, echocardiographic and hemodynamic correlates. 646 7

Aortic stenosis is a heritable cardiac anomaly most common in German Shepherds, Boxers and Newfoundlands, and less common in Pugs, English Bulldogs, Boston Terriers, Fox Terriers, Schnauzers and Bassets. Clinical signs are associated with secondary left-sided heart failure and include coughing, moist rales, exercise intolerance, arrhythmias and a weak femoral pulse. It causes an ejection-type crescendo-decrescendo, systolic murmur best heard on the left side near the elbow. The ECG may be normal or may show signs of left ventricular hypertrophy, including an axis of less than 40 degrees, a QRS complex of greater than 60 seconds in duration, R waves greater than 3 mv in amplitude, ST segment slurring or depression, or T waves of an amplitude greater than 25% of that of R waves. A LAT radiograph usually reveals an enlarged cardiac silhouette, loss of the cranial cardiac waist, and normal pulmonary vasculature, while DV projections show an elongated cardiac silhouette, rounding of the left ventricular border, and a normal descending aorta. Nonselective angiocardiography reveals poststenotic dilatation of the aorta. Treatment of severely affected dogs involves surgical correction.
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PMID:Congenital cardiac disease in dogs. 648 69

To investigate the usefulness of stress testing for the evaluation of hypertensive heart disease, 40 subjects, 28 men and 12 women (mean age 30.8 +/- 6.2 years), with mild or moderate hypertension, without ST segment or T wave abnormalities in their resting ECG, were examined. 13 patients (32.5%) showed exercise-induced ST segment depression. The heart rate at rest was significantly higher in the patients with a positive response; 6 of the 7 subjects with electrocardiographic signs of left ventricular hypertrophy (summed SV1 + maximum R V5/V6 voltage of 45 mm or more) had a positive exercise electrocardiographic test. There were no significant differences between positive and negative cases in age, sex, systolic and diastolic blood pressure, or the double product (heart rate X systolic pressure) at rest or during exercise. After resting blood pressure values had been significantly decreased by giving methyldopa with or without diuretics for at least 6 months, there were a regression of left ventricular hypertrophy in the resting ECG and an impressive reduction in the prevalence of exercise-positive responses (to 17.5%). In the 7 patients with positive exercise electrocardiographic tests even after antihypertensive treatment, no significant reduction in blood pressure values during exercise was obtained.
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PMID:Usefulness of stress testing for the evaluation of hypertensive heart disease in young hypertensive subjects. 648 27


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