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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several intracellular enzymes have been shown to have altered total activity or isoenzyme composition in cardiac hypertrophy. This study tests the hypothesis that the accumulation of the fetal-type (BB + MB) creatine kinase (CK) isoenzymes in hypertrophied adult myocardium is related to an increase in blood pressure. Consideration was made for the location, size, and hemodynamic load of the myocytes. By using the two-kidney, one-clip (2K1C) rat model of renal hypertension with and without hydralazine treatment, CK (total and isoenzyme), lactate dehydrogenase, and citrate synthase activities and myocyte size were measured. An increased heart weight/body weight ratio occurred in both untreated 2K1C rats (4.15 +/- 0.09) and hydralazine-treated 2K1C rats (4.12 +/- 0.13) as compared with control rats (3.25 +/- 0.10). Blood pressure was high only in untreated 2K1C rats (196 +/- 9 mm Hg), as compared with hydralazine-treated 2K1C rats (142 +/- 6 mm Hg) and control rats (135 +/- 3 mm Hg). Myocytes were isolated from five ventricular regions: left ventricular epicardial and endocardial free wall, left and right halves of the interventricular septum, and right ventricular free wall. Regional differences in normal and hypertrophied myocardium were demonstrated for morphological and biochemical parameters, with the greatest changes occurring in left ventricular endocardium. The shift in CK isoenzyme expression toward accumulating more BB + MB was greater in "hypertensive hypertrophy" (untreated 2K1C rats) than in "nonhypertensive hypertrophy" (hydralazine-treated 2K1C rats). Calculations incorporating isolated myocyte volume showed that the cellular content of total CK remained the same during the hypertrophic process, accounting for a decrease in the tissue activity. Measurement of lactate dehydrogenase and citrate synthase activities suggests that hypertrophied myocardium has relatively higher glycolytic capacity and that this effect is exacerbated in the presence of high blood pressure. We conclude that increased blood pressure is more closely linked to the fetal CK isoenzyme shift than is hypertrophy alone.
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PMID:Regional changes in creatine kinase and myocyte size in hypertensive and nonhypertensive cardiac hypertrophy. 214 29

We tested the hypotheses that after complete cerebral ischemia, first, rate of recovery of ATP, phosphocreatine (PCr), and intracellular pH (pHi) varies with ischemic duration and second, rate of metabolic recovery is a more sensitive predictor of consequent electrophysiological deficit than steady-state metabolic recovery. With the use of transient intracranial hypertension in anesthetized dogs, ischemic duration was set for either 3, 12, or 30 min, which depressed somatosensory-evoked potential (SEP) recovery amplitude by 30, 59, and 88%, respectively. In contrast, ATP, PCr, and pHi, measured by 31P magnetic resonance spectroscopy, fully recovered. When ischemic duration was increased from 3 to 12 min, mean recovery time of ATP (6 min) remained rapid but that of pHi (12-28 min) was prolonged. After 30 min of ischemia, pHi recovery was not slowed further (25 min) but that of ATP was now markedly prolonged (36 min). PCr recovery time increased progressively with ischemic duration (5, 11, and 21 min, respectively) and correlated best with SEP recovery (r = 0.74). We conclude that the brain's ability to rapidly normalize pH is a sensitive predictor of electrophysiological recovery after short ischemia but that ATP regeneration becomes important with prolonged ischemia. PCr recovery rate was the best overall predictor, probably because it depends on both pHi and the ratio of ATP to ADP by the creatine kinase reaction.
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PMID:Postischemic recovery rate of cerebral ATP, phosphocreatine, pH, and evoked potentials. 251 29

In the myocardium, myosin and creatine kinase isoforms possess different capacities for using O2 and energy-rich phosphates. We studied electrophoretically the distribution of these isoforms in 19 hypertensive rats (two-kidney, one clip model of hypertension) and in age-matched controls. After 6 weeks of hypertension, seven rats were treated with captopril (2 mg/kg daily) for 4 weeks, six were left hypertensive for another 4 weeks, and the remaining rats were killed under ether anesthesia. In the latter, ventricular mass was significantly higher than in controls; V3 isomyosin was 32.3 +/- 6.8% versus 0%, and both creatine kinase-MB and -BB were increased at the expense of creatine kinase-MM (creatine kinase-MB = 29 +/- 2.8% vs. 14.7 +/- 1.8%, p less than 0.001; creatine kinase-BB = 3.1 +/- 0.6% vs. 1.7 +/- 0.8%, p less than 0.001). After 10 weeks of hypertension, ventricular mass, V3 isomyosin, and both creatine kinase-MB and -BB isoforms were found to be persistently higher than in controls. At the same time, captopril-treated rats showed reduced but not normalized blood pressure levels, normalized ventricular mass, and prevalence of the V1 isomyosin (56.9 +/- 22% vs. 47.9 +/- 23.8% in normotensive controls, p = NS). However, higher levels of creatine kinase-MB and -BB were still found in these rats in comparison with the normotensive controls (creatine kinase-MB = 22.4 +/- 5.4% vs. 15.8 +/- 2.8%, p less than 0.025; creatine kinase-BB = 2.3 +/- 0.1% vs. 1.8 +/- 0.3%, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Nov
PMID:Ventricular myosin and creatine-kinase isoenzymes in hypertensive rats treated with captopril. 268 Sep 63

Malignant hyperthermia (MH) is a pharmacogenetic disease in man and animals. It primarily involves skeletal muscle tissue, but other tissues might be affected to a lesser degree. Calcium homeostasis in muscle cells is upset in susceptible individuals, so that various agents and circumstances can increase the free, ionised intracellular calcium concentration to damaging levels. The primary defect is not known at present, but is believed to involve an abnormally sensitive calcium-induced calcium release mechanism. Thus small, localised increases in calcium concentration releases more calcium so that a vicious cycle is triggered. The increased calcium concentration causes multiple effects in the muscles by stimulating contraction and a hypermetabolic state, clinically observed as rigidity and fever. If demands on the homeostatic mechanisms to lower the calcium concentration become exhausted, and metabolism is insufficient to supply enough phosphocreatine and ATP, membrane potentials cannot be maintained, and permeability of the cell membranes increase. This causes loss of phosphate and H+ as well as K+ and Mg++, and later myoglobin and creatine kinase. Thereby oxidative metabolism is further impeded with formation of lactate as a result. The ensuing acidosis stimulates sympathetic innervation, resulting in tachycardia, high blood pressure, and vasoconstriction. Hyperkalemia causes arrhythmia. Dantrolene inhibits the release of calcium and can halt the process if given before depletion of the energy rich phosphates is too advanced.
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PMID:Pathophysiology of malignant hyperthermia. 269 55

To investigate the pathophysiologic relevance of angiographically irregular coronary stenoses in postinfarction angina (PIA), we analyzed the clinical course and coronary angiograms of 73 patients studied within 30 days of infarction. Coronary lesions were classified as smooth or irregular. Thirty-six patients had PIA (Group 1) and 37 had an uncomplicated course (Group 2). Irregular lesion(s) in patent infarct-related arteries were found in 77% of Group 1 vs. 24% of Group 2 patients (P less than 0.005). Irregular lesion(s) in any coronary artery were found in 58% of Group 1 versus 19% of Group 2 patients (P less than 0.002). Other univariate predictors of PIA included older age, hypertension, angina before myocardial infarct, lower peak creatine kinase, three-vessel disease, and higher modified Gensini score. Multivariate analysis ranked lesion irregularity as the strongest predictor of PIA. Our data suggests that ruptured atherosclerotic plaques may be important in the pathogenesis of PIA. It is possible that lesion irregularity is associated with an active process and/or a residual thrombus, which may be responsible for postinfarction angina.
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PMID:Angiographic coronary morphology in postinfarction angina. 292 Mar 88

Diabetes mellitus has been associated with high mortality rates in patients with acute myocardial infarction (AMI). To better define prognosis in this population, the clinical course of 183 diabetics with AMI was studied. In-hospital mortality for all patients was 28% (52 of 183 patients). Mortality was significantly higher in patients with prior AMI than in patients without prior AMI (41 vs 18%, p less than 0.01) and was significantly higher in women than in men (37 vs 19%, p less than 0.01). The 2-fold increase in mortality among diabetic women was observed both in patients with and without prior AMI. The excess mortality among diabetic women was attributable to their increased risk for severe congestive heart failure (CHF) and cardiogenic shock. Death due to CHF occurred in 22% of all diabetic women with AMI compared with 6% of the diabetic men (p less than 0.01). Death resulting from complications other than CHF was similar for both sexes. There were no male-female differences in the history of prior AMI, systemic hypertension, obesity, nephropathy, frequency of Q-wave AMI, anterior AMI or peak creatine kinase levels to account for the high risk for CHF in diabetic women. It is therefore concluded that diabetic women with AMI are at increased risk for death due to CHF, and that this risk is not readily attributable to known conditions associated with CHF.
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PMID:Acute myocardial infarction in diabetes mellitus and significance of congestive heart failure as a prognostic factor. 342 Nov 62

A young woman taking tranylcypromine for depression was hospitalized with severe chest pain and hypertension after eating cheese. Electrocardiography initially showed arrhythmias and precordial ST segment depression. Myocardial creatine kinase values were elevated, and echocardiography showed regional ventricular dysfunction, suggestive of focal cardiac myonecrosis. The cardiovascular pathophysiology of tyramine hypertensive crisis and related catecholamine excess states, including pheochromocytoma and clonidine withdrawal, is reviewed. Cardiac myonecrosis is a potential adverse effect of the hypertensive crisis associated with monoamine oxidase inhibitor use. Psychiatric indications for monoamine oxidase inhibitors may be expanding, but clinicians should continue to exercise caution in the use of these agents.
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PMID:Cardiac myonecrosis in hypertensive crisis associated with monoamine oxidase inhibitor therapy. 357 43

To identify patients at risk of cardiac expansion during hospital stay for a first acute myocardial infarction (AMI), 41 patients underwent right-sided cardiac catheterization soon after admission and serial 2-dimensional echocardiography on days 1, 3 or 4 and between days 7 and 10. Infarct expansion was recognized by echocardiography in 11 patients (27%), most often on the second recording (day 3 or 4). Age, sex, time from onset of pain to catheterization, peak levels of creatine kinase and creatine kinase-MB isoenzyme, heart rate, mean pulmonary artery wedge pressure and left ventricular stroke work index were similar in the 2 groups. Patients in whom infarct expansion developed had a higher incidence of previous systemic hypertension (73% vs 27%, p less than 0.01) and anterior AMI (91% vs 30%, p less than 0.001) and a higher mortality rate at 1 year (73 vs 7%, p less than 0.001) than those who did not. They also had higher systolic (139 +/- 24 vs 126 +/- 18 mm Hg, p less than 0.05) and diastolic (91 +/- 14 vs 75 +/- 13 mm Hg, p less than 0.001) arterial pressures, lower stroke volume index (31 +/- 10 vs 40 +/- 10 ml/m2, p less than 0.01) and much higher systemic vascular resistance (SVR) values (1,713 +/- 380 vs 1,253 +/- 264 dynes s cm-5, p less than 0.0001). In the subgroups of patients with anterior AMI, differences were significant for diastolic arterial pressure, stroke volume index, SVR and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic profile of patients with acute myocardial infarction at risk of infarct expansion. 360 44

Detailed drinking histories were taken in 38 patients in whom dilated cardiomyopathy was diagnosed by cardiac catheterisation and left ventricular biopsy. On the basis of the drinking history twenty patients were classified as being in an abstinent or light drinking group and eighteen patients as being in a heavy drinking group (daily alcohol intake in excess of 80 g or cumulative lifetime intake exceeding 250 kg). Activities of myocardial creatine kinase, lactate dehydrogenase, alpha hydroxybutyric dehydrogenase, malic dehydrogenase, and aspartate amino-transferase were all higher in the heavy drinkers and myocardial enzyme activity correlated with cumulative lifetime alcohol intake, maximum daily intake, and recent daily intake. Activities of creatine kinase, alpha hydroxybutyric dehydrogenase, and malic dehydrogenase correlated with ejection fraction, irrespective of the alcohol intake of the patient. These findings were not altered by exclusion of patients with hypertension. The results indicate that among patients with dilated cardiomyopathy there is a group characterised by a high alcohol intake and raised myocardial tissue enzymes which supports the concept of alcoholic heart muscle disease as a distinct entity.
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PMID:Relation between alcohol intake, myocardial enzyme activity, and myocardial function in dilated cardiomyopathy. Evidence for the concept of alcohol induced heart muscle disease. 373 Feb 17

Total creatine kinase was measured in serum samples obtained from 307 asymptomatic healthy subjects, 112 men and 195 women, during screening visits to the Yale University Hypertension Clinic or the Yale-New Haven Hospital Primary Care Center or during pre-employment physical examinations at the Yale-New Haven Hospital Personnel Health Clinic. The group consisted of 147 blacks, 132 whites, and 28 Hispanics. Blood pressure was measured in all patients, and weight, height, and serum potassium and creatinine levels were determined in most. Any subject who had engaged in any vigorous exercise in the 12 hours prior to the visit was excluded. The mean total creatine kinase level for black men was 146.5 +/- 136.9 units/liter (median, 108 units/liter), the mean level for white men was 60.8 +/- 26.1 units/liter (median, 51 units/liter), and the mean level for Hispanic men was 84.5 +/- 70.6 units/liter (median, 57 units/liter). The mean level for black women was 66.4 +/- 50.0 units/liter (median, 53 units/liter), the mean level for white women was 37.0 +/- 18.2 units/liter (median, 32 units/liter), and the mean level for Hispanic women was 41.5 +/- 36.0 units/liter (median, 30 units/liter). Using the testing laboratory's normal values for total creatine kinase (8 to 80 units/liter for men and 5 to 50 units/liter for women), 37 black men (64.9 percent) and 49 black women (54.4 percent) had abnormal values for total creatine kinase. Although sex, race, diastolic blood pressure, serum creatinine level, and presence of hypertension correlated significantly with total creatine kinase levels in the entire population, only sex did so in blacks. Multivariate analysis using linear regression techniques clearly demonstrated that sex and race were the only variables that independently predicted the total creatine kinase level. These findings show that healthy asymptomatic blacks have higher total creatine kinase levels than whites or Hispanics, with the majority having values in the abnormal range. Thus, different normal values should be used for blacks, just as they are for men and women, and elevated total creatine kinase levels should be interpreted with considerable caution.
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PMID:Racial differences in serum creatine kinase levels. 375 49


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