Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Blood pressure measurements were recorded in 522 adults and 141 10-19 year-old full and part blood Aborigines in five communities. The means for systolic and diastolic blood pressures at 40 years were close to those reported for Europeans, although below this age, values tended to be lower, and above 40 years tended to be higher than those reported in the Tecumseh study. Hypertension, as defined by the Princeton criteria, was present in 29%, more often in the men (1-6 to 1-0), and eight subjects satisfied the criteria for hypertensive heart disease (HHD). 522 electrocardiograms were recorded on adult subjects at five Aboriginal communities and classified according to categories of the Minnesota code. Of the 210 abnormalities observed, minor T wave inversions and minor S-T segment depression were the most commonly encountered, and were more frequent in female subjects. Q wave changes typical of myocardial infarction was found in 5% of the tracings and occurred mainly in older men. If hypertension and certain ECG codes are assumed to be "risk factors" for the development of clinical ischaemic heart disease (IHD), the urbanized Aboriginal had a higher prevalence compared with Caucasian subjects of the Busselton study. "Probable" and "suspect" ECG changes of IHD, although mainly in the older subjects, were found to be associated with hyperglycaemia, as recognised in Western society. It is postulated that urbanized Aborigines are prone to cardiovascular degenerative disease to a similar or possibly larger extent than Caucasians.
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PMID:Blood pressures and electrocardiographic findings in the South Australian Aborigines. 106 18

To determine whether myocardial ischemia is accompanied by variation in heart rate and/or blood pressure, ST-segment analysis on Holter-ECG and ambulatory blood pressure monitoring was performed in 78 patients (64 males/14 females) with essential hypertension. Thirteen out of 55 patients (24%) with angiographically proven coronary artery disease (CAD) showed ST-segment depression (ST-D; group A pos). We observed 41 ST-D (1-11 ST-D; median: 2) lasting from 1 min to 70 min 15 s (median: 4 min 42 s) and an average depression of 185 +/- 48 mV. In comparison, in 6 of 23 patients (26%) with a normal angiogram 24 ST-D (1-10; median: 3; group B pos), which showed longer duration (1 min to 109 min 20 s; median: 11 min 10 s) and less depression (137 +/- 47 mV) have been found. 73.3% of all ST-D in group A pos and all in group B pos were preceded by an average increase in heart rate of 13 bpm. Exclusively, 12 episodes of ischemia (29.3%) in patients with CAD and 8 (33.3%) in patients without CAD were accompanied by an increase in blood pressure, which was more distinct in group A pos. Transient myocardial ischemia can be shown in hypertensive heart disease unrelated to CAD. A clear correlation between an increase in blood pressure and ST-D could not be proven.
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PMID:[Blood pressure variability and transient myocardial ischemia in patients with essential hypertension]. 151 10

An impaired coronary vasodilator reserve has been demonstrated in all stages of hypertensive heart disease but is most likely in the setting of hypertrophy. The decrease in coronary flow reserve has, however, not been predictable previously. We postulated that flow reserve depression might be related to a left ventricular mass threshold. Seventy-two patients (82% with hypertension) with suspected ischemic heart disease who were found to be free of significant coronary artery disease at cardiac catheterization were evaluated utilizing the intracoronary Doppler catheter and two-dimensional directed M-mode echocardiography for determination of coronary flow reserve and left ventricular mass. For left ventricular mass indexed (LVMI) by body surface area (BSA) greater than or equal to 50% above normal using established gender-specific norms, American Society of Echocardiography (ASE) and PENN methods (correction of LV mass by regression equation agreeing with necropsy estimates of mass) predicted impairment of flow reserve (p = 0.005 and 0.009, respectively). Unindexed left ventricular mass and LVMI by height were not helpful in this regard. Using the ASE method for LV mass determination, coronary flow reserve was moderately depressed (2.4 +/- 1.0) for those with LVMI greater than or equal to 50% above normal; in comparison, flow reserve was normal (3.5 +/- 1.3) for those with LVMI less than 50% above normal. A rare patient was able to maintain a normal flow reserve when ASE- and Penn-indexed mass estimates were greater than or equal to 50% above normal, but only in the setting of a markedly elevated mean arterial pressure.
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PMID:Relationship of left ventricular mass to impairment of coronary vasodilator reserve in hypertensive heart disease. 182 83

In hypertensive heart disease without coronary artery disease it has been proposed that the presence of ischemia of myocardial tissue is due to an inadequate increment of myocardial mass or to an increase in coronary artery resistance. In this study, 18 patients with aortic stenosis, without coronary artery disease were included. It was demonstrated that the existence of myocardial ischemic, induced by atrial pacing and manifested by ST segment depression, had direct association to increased myocardial mass, and it had no relation with left ventricular telediastolic pressure nor with transvalvular gradient. The results support the hypothesis that an inappropriate increment of the myocardial mass is the main cause of myocardial ischemia in these type of cardiopathies.
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PMID:[Myocardial ischemia in aortic stenosis]. 253 25

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

With the correct selection of drug and patient, the calcium antagonists as a group can be remarkably effective at relatively low cost of serious side effects. Almost all side effects are dose related. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil (or diltiazem) is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine which actually has the most marked negative inotropic effect. Yet caution is required when even calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide. The most marked interaction with digoxin is that with verapamil, which may raise digoxin levels by over 50%. Combination therapy of calcium antagonists with beta-blockers is increasingly common, and is probably safest in the case of dihydropyridines. Other combinations being explored are those with angiotensin-converting enzyme inhibitors and diuretics.
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PMID:Calcium channel antagonists. Part IV: Side effects and contraindications drug interactions and combinations. 315 4

The hemodynamic and contractile effects of clonidine were studied in hypertrophied hearts of spontaneously hypertensive rats (Okamoto-Aoki strain, SHR). The hemodynamic pattern was characterized by dose-dependent decreases in systolic blood pressure and systolic wall stress, ie, the afterload imposed upon the left ventricle, whereas left ventricular ejection fraction and stroke volume were unchanged. Even at extremely high doses (10(-5)M/L) there was found no depression of isometric tension development and maximum isotonic shortening velocity of the isolated LV papillary muscle. It is concluded that clonidine may be beneficial in hypertensive heart disease, if ventricular unloading associated with a reduction in myocardial energy demand is desired.
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PMID:The role of clonidine in hypertensive heart disease. Influence on myocardial contractility and left ventricular afterload. 621 55

Sixty four patients with essential hypertension were studied by phonocardiographic systolic time intervals. Prolongation of the pre-ejection period (PEP) at expense of the isovolume contraction time and of the true isovolume contraction time, which suggests myocardial contractile depression due to the increase in after-load. The significant increase, in rise of mean velocity of ventricular pressure suggests that the Anrep phemomena is used by the human heart as a compensatory mechanism in systemic hypertension. Ejection fraction in hypertensives was significantly lower (P less than 0.001) than that of normal controls, which indicates subclinical depression of ventricular function in the former. Myocardial hypertrophy can be considered as a compensatory mechanism which appears late in systemic hypertension and helps normalize ventricular performance and MVO2. It is clinically detected by an s-4 (registered by phonocardiographic tracings) and by an increase in the "A" index and the apexcardiogram (14.5 +/- 8%). The authors conclude that hypertensive heart disease can be identified early through the functional adaptations wich produce detrimental physiopathological reactions to the heart compensated initially by homeometric autorregulation and latter by myocardial hypertrophy.
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PMID:[Hypertensive cardiopathy. Phonomechanocardiographic study and review of its physiopathological mechanisms]. 622 4

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


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