Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to investigate the plasma concentration of atrial natriuretic peptide (ANP) in acute myocardial infarction (AMI), its association with age, sex, essential hypertension, infarct localization, complications of AMI, infarct size, left atrial and ventricular chamber sizes and therapy of AMI. I studied 40 pts (9 female, 31 male, mean 56.9 + 10 years) with first AMI up to 6 hours onset the first symptoms (mean 2.4 + 1.2 hours). The ANP concentration was measured at the time of admission to the hospital (ANP 0) and at time 4, 8, 16, 24, 48, 72 hours after admission (ANP mean). Arrhythmias was assessed by 24 hour ecg Holter monitoring. Infarct size was assessed by serial CK-MB measurement in first 72 hours of AMI. Contractility disturbances and left atrial and ventricular chamber sizes was assessed by echocardiography. The average plasma concentration of ANP was significantly elevated (28.1 +/- 4.3 fmol/ml). The mean ANP concentration was significantly higher in pts with essential hypertension than in pts without hypertension (36.1 + 7.7 vs 21.7 + 4.2 fmol/ml). The ANP concentration in pts with inferior myocardial infarction was significantly higher than in pts with anterior myocardial infarction (32.1 + 6.1. vs 20.9 + 4.1 fmol/ml). The ANP mean in pts with complications of AMI (congestive heart failure, arrhythmias, reinfarction, death) was significantly higher than in pts without complications (49.5 + 13.3 vs 21.6 + 7.1 fmol/ml). I observed positive correlation between plasma ANP and left atrial chamber sizes (r = 0.59) and diastolic ventricular dimension (r = 0.56).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial natriuretic peptide in patients with acute myocardial infarction]. 812 91

We report the case of a 70 years-old patient admitted for an acute anterior myocardial infarction and who subsequently presented postprandial episodes of astenia, dyaphoresis and arterial hypertension associated with re-elevation of the ST segment and positivization of T waves in the precordial leads, without chest pain. These episodes were interpreted as silent postprandial myocardial ischemia. A coronary angiography demonstrated a single vessel disease with a severe and proximal stenosis of the left descending coronary artery which was successfully dilated during angioplasty. However, the postprandial episodes persisted and re-estenosis was ruled out in a repeated coronary angiogram. A stress thallium myocardial scintigraphy was negative. Complementary tests documented the existence of a pheochromocyctoma and the refered postprandial symptoms did not recur after removal of the tumor. Thus, the persistence of postprandial episodes of myocardial ischemia associated with severe hypertension and dyaphoresis in the absence of a significant coronary stenosis, may possibly be related to a concomitant coronary and systemic vasoconstriction secondary to the adrenal tumor.
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PMID:[Pheochromocytoma, acute myocardial infarction and silent postprandial ischemia]. 868 16

Angiotensin converting enzyme (ACE) inhibitors have emerged as the class of antihypertensive and vasodilatatory agents of first choice in the treatment of elderly patients with hypertension. Normotensive patients with congestive heart failure, post-anterior myocardial infarction, or diabetes mellitus with evidence of microangiopathy will also benefit from continuous ACE inhibition. The long term use of ACE inhibitors is associated with improved survival and reduced cardiovascular, cerebral and renal morbidity in these patients. In elderly atherosclerotic patients, these agents provide good control of systolic and diastolic blood pressure and peripheral resistance, with remarkable preservation of vital organ perfusion and infrequent adverse effects. Used as monotherapy, the effectiveness of ACE inhibitors is limited. However, there are advantages for using them in combination with other drugs, notably thiazide diuretics, nitrates and calcium antagonists. Renal function is thus preserved and left heart hypertrophy is prevented. There are no major differences between the various ACE inhibitors, and the choice of drug is largely a matter of personal preference.
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PMID:ACE inhibitors in elderly patients with hypertension. Special considerations. 878 66

To investigate the role of left ventricular (LV) diastolic function in the maintenance of exercise capacity in patients with systolic dysfunction, symptom-limited cardiopulmonary exercise testing combined with radionuclide ventriculography was performed in 24 patients with an LV ejection fraction < 35% after anterior myocardial infarction. The ratio of pulmonary artery wedge pressure (PAWP) to LV end-diastolic volume (EDV), an index of global diastolic function, correlated significantly with peak oxygen consumption at peak exercise (r = -0.55; p = 0.006), whereas ejection fraction at peak exercise did not. The change in PAWP/EDV ratio from rest to peak exercise was related to the increases in stroke volume (r = -0.54; p = 0.006) and cardiac output (r = -0.51; p = 0.01) during exercise, but the change in ejection fraction was not. Resting hemodynamics did not differ between patients with preserved exercise capacity (group 1, n = 8) and those with exercise impairment (group 2, n = 16). At peak exercise, stroke volume, cardiac output, and EDV were significantly higher, and PAWP and PAWP/EDV ratio were significantly lower in group 1 than in group 2, but ejection fraction and end-systolic volume were similar in both groups. Although the incidences of hypertension, LV hypertrophy, and infarct-related coronary artery lesions did not differ between the two groups, group 2 had a significantly higher incidence of non-infarct-related coronary artery lesions than group 1 (p < 0.05). Thus in patients with LV systolic dysfunction after anterior myocardial infarction, the major cause of exercise impairment and failure to increase LV performance during exercise was diastolic dysfunction associated with the presence of non-infarct-related coronary artery lesions with the potential for exercise-induced ischemia of the noninfarcted areas.
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PMID:Importance of left ventricular diastolic function on maintenance of exercise capacity in patients with systolic dysfunction after anterior myocardial infarction. 900 95

Which patients with an acute myocardial infarction should be treated with an angiotensin-converting enzyme (ACE) inhibitor and when should this treatment be initiated? Combining pathophysiological evidence with the findings of large clinical trials, it is recommended that in the postinfarction setting ACE inhibitors should be given only to high risk patients, ie, patients with arterial hypertension, patients in Killip class II or III, patients with an acute anterior myocardial infarction, patients with left ventricular dysfunction and patients with a previous myocardial infarction. Treatment should be started as soon as it is considered safe.
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PMID:A pragmatic approach to the use of angiotensin-converting enzyme inhibitors in acute myocardial infarction. 919 82

We investigated the effects of endothelin-1 on pressor responses to norepinephrine in perfused mesenteric arteries of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The response to norepinephrine (10(-6) M) was significantly increased in DOCA-salt rats compared with that in uninephrectomized control rats. Perfusion of the arteries with subpressor dose of endothelin-1 (3 x 10(-10) M) for 15 min markedly enhanced the pressor responses to norepinephrine (10(-6) and 3 x 10(-6) M) in control rats and this effect was significantly prevented by BQ788 [N-cis-2,6-dimethylpiperidinocarbonyl-L-gamma-methylleucyl-D -1-methoxycarbonyl-tryptophanyl-D-norleucine] (10(-6) M), but not by FR139317 ((R)2-[(R)-2-[(S)-2-[[1-(hexahydro-1H-azepinyl)]carbonyl]amino-4-+ ++methylpentanoyl]amino-3-[3-(1-methyl-1H-indoyl)]propionyl]ami no-3-(2-pyridyl)propionic acid) (10(-6) M). In DOCA-salt hypertensive rats, increased pressor response to norepinephrine was declined to the level of control rats by BQ788, but not by FR139317. In contrast to the case seen with control rat, exogenous endothelin-1 had little effect on pressor responses to norepinephrine in the arteries of DOCA-salt hypertensive rats. Total immunoreactive endothelin content in the arteries of DOCA-salt hypertensive rats was significantly higher than that of uninephrectomized control rats. These results suggest that endothelin-1 enhances contractile responses to norepinephrine through endothelin ETB receptor. Moreover, this phenomenon is stimulated tonically by endogenous endothelin-1 in DOCA-salt hypertensive rats and may contribute to the maintenance of hypertension in DOCA-salt rats.
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PMID:Effects of endothelin-1 on norepinephrine-induced vasoconstriction in deoxycorticosterone acetate-salt hypertensive rats. 957 Apr 48

Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. For vascular endothelium, hepatocyte growth factor (HGF) is one of the most potent and specific growth factors, which acts protectively against endothelial dysfunction. HGF production is downregulated by angiotensin II (Ang II) in vitro. We hypothesized that HGF production is impaired as the result of increased Ang II in patients with congestive heart failure, and that if so, the impaired production should be restored with angiotensin-converting enzyme inhibitors (ACE-I). We studied 16 patients with congestive heart failure caused by previous anterior myocardial infarction in whom left ventricular ejection fraction was 35+/-8% (mean+/-SD). Before and approximately 4 weeks after the treatment with ACE-I, blood samples were collected to measure the levels of HGF, Ang II, and brain natriuretic peptide as a biochemical marker for severity of heart failure. We also studied 5 control subjects, in whom heparin increased HGF production to 48+/-5-fold. However, in patients with heart failure, HGF response to heparin was significantly attenuated (24+/-5-fold, P<0.05 vs control). Therapy with ACE-I decreased the levels of Ang II and brain natriuretic peptide and restored HGF production in response to heparin by 43+/-7-fold, comparable to the control response. In conclusion, impaired HGF production was restored after the treatment with ACE-I probably by the mechanism of Ang II suppression. This novel effect of ACE-I may contribute to the clinical improvement in patients with heart failure and thereby may have an important therapeutic implication.
Hypertension 1999 Jun
PMID:Angiotensin-converting enzyme inhibition restores hepatocyte growth factor production in patients with congestive heart failure. 1037 19

This study determines the usefulness of electrocardiography in the emergency room for assessing the risk of cardiac rupture after acute anterior myocardial infarction (MI). The presence of ST segment elevation on the admission 12-lead electrocardiography was evaluated in 325 consecutive anterior MI patients. A forward-stepwise logistic regression analysis for cardiac rupture was performed with the covariates of age, gender, hypertension, history of MI, reperfusion therapy by coronary angioplasty, and ST segment elevations in leads I, aVL, V1-V6. Cardiac rupture occurred in 16 patients, including 7 with left ventricular free wall rupture (FWR) and 9 with ventricular septal perforation (VSP). For FWR, ST elevation in lead aVL was the only independent predictor (odds ratio = 12.1, P = .0215). For VSP, female gender (odds ratio = 5.32, P = .0201) was the independent predictor. In conclusion, in patients with acute anterior MI, ST segment elevation in lead aVL on the admission electrocardiography is a significant risk factor for left ventricular FWR.
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PMID:Cardiac rupture and admission electrocardiography in acute anterior myocardial infarction: implication of ST elevation in aVL. 1069 Nov 74

Complete right and left bundle branch block and advanced atrioventricular block present on admission electrocardiograms of patients with acute myocardial infarction, are associated with poor short and long-term outcome. Little is known about the impact of intermediate QRS prolongation (0.09-0.11 s) on the prognosis of acute myocardial infarction. In this study, among 1100 consecutive patients with acute myocardial infarction treated with thrombolysis, the QRS duration on admission electrocardiogram was <0.09 s in 536 (48%) patients, between 0.09 and 0.11 s in 496 (45%) patients and >0.11 s in 78 (7%) patients. QRS duration was strongly associated with 7-day (0.6%, 6%,18%, P<0.001), 30-day (1%, 8%, 22%, P<0.001) and 1-year (3%, 11%, 26%, P<0.001) all-cause mortality. After adjustment for significant variables associated with 1-year mortality, including age, female gender, diabetes mellitus, systemic hypertension, previous myocardial infarction, anterior myocardial infarction and Killip class> or =2 on admission, both levels of QRS prolongation remained significant independent predictors of short and long-term all-cause mortality.
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PMID:The prognostic significance of intermediate QRS prolongation in acute myocardial infarction. 1137 26

We report the case of a 40-year-old HIV-positive man, undergoing three-drug antiretroviral therapy for 2 years that included a protease inhibitor (ritonavir). The patient was admitted to our Coronary Care Unit with an acute anterior myocardial infarction. He smoked 20 cigarettes/day and had a family history of hypertension. At the time of hospitalization, triglyceride levels were found to be high (290 mg/dl). Metabolic alterations associated with the prolonged use of protease inhibitors, such as insulin resistance, dyslipidemia and lipodystrophy, have recently been described. This side effect may lead to premature coronary artery disease. Therefore it is mandatory to be aware that treatment with protease inhibitors in HIV-positive patients, despite survival prolongation and lowering of AIDS complications, may accelerate atherosclerosis and precipitate acute coronary events, especially in patients with pre-existing cardiovascular risk factors.
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PMID:[Acute myocardial infarct in HIV-positive patients in treatment with protease inhibitors]. 1177 17


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