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

We previously found mild hypothermia (34-36 degrees C), induced before cardiac arrest, to improve neurologic outcome. In this study we used a reproducible dog model to evaluate mild hypothermia by head cooling during arrest, continued with systemic cooling (34 degrees C) during recirculation and for 1 h after arrest. In four groups of dogs, ventricular fibrillation (no flow) of 12.5 min at 37.5 degrees C was reversed with cardiopulmonary bypass and defibrillation in less than or equal to 5 min, and followed by controlled ventilation to 20 h and intensive care to 96 h. In Study A we resuscitated with normotension and normal hematocrit; Control Group A-I (n = 12) was maintained normothermic, while Treatment Group A-II (n = 10) was treated with hypothermia. In Study B we resuscitated with hypertension and hemodilution. Control Group B-I (n = 12) was maintained normothermic (6 of 12 were not hemodiluted), while Treatment Group B-II (n = 10) was treated with hypothermia. Best overall performance categories (OPCs) achieved between 24 and 96 h postarrest were in Group A-I: OPC 1 (normal) in 0 of 12 dogs, OPC 2 (moderate disability) in 2, OPC 3 (severe disability) in 7, and OPC 4 (coma) in 3 dogs. In Group A-II, OPC 1 was achieved in 5 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.001), OPC 3 in 1, and OPC 4 in 0 dogs. In Group B-I, OPC 1 was achieved in 0 of 12 dogs, OPC 2 in 6, OPC 3 in 5, and OPC 4 in 1 dog. In Group B-II, OPC 1 was achieved in 6 of 10 dogs (p less than 0.01), OPC 2 in 4 (p less than 0.05), and OPC 3 or 4 in 0 dogs. Mean neurologic deficit and brain histopathologic damage scores showed similar significant group differences. Morphologic myocardial damage scores were the same in all four groups. We conclude that mild brain cooling during and after insult improves neurologic outcome after cardiac arrest.
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PMID:Mild cerebral hypothermia during and after cardiac arrest improves neurologic outcome in dogs. 229 37

The purpose of this study was to investigate, if besides the hypocontractility, which is the main finding in Primary Cardiomyopathy (PDC) there was some other mechanism in the development of heart failure and if this fact could influence in it's prognosis. We studied 13 patients with PDC in the hemodynamic cardiac laboratory from January 1982 to January 1988, these with systemic arterial hypertension. Coronary heart disease, myocarditis, primary valvular lesion, infiltrative disease, nephropathy, congenital heart disease, diabetes and alcoholism, were excluded. The control group was formed by 12 healthy subjects, which were studied for another purpose. We analyzed nine variables, including ejection fraction, peripheral vascular resistance, systolic and diastolic circumferential stress, left ventricular mass, left ventricular end diastolic and systolic volumes as well as force-velocity and force-fiber length relationship. The patients were followed up from 8 to 60 months (average 39 months). The cases with PDC were divided in two groups, "compensated" and "decompensated". The last ones with low ejection fraction and significantly increases systolic stress. We investigated which was the mechanism of compensation and decompensation through the force-velocity and force-fiber length relation. We found that compensation is associated with great increase of the after-load forces, the more end systolic volume at the end of the systole is not only controlled by the "force", but the decompensation is developed when the hypocontractility is added to the incompetence to compensate the after load. We found that the three deaths in this study had these hemodynamic characteristics, being the cause of death: the presence of heart failure in two patients and ventricular fibrillation in one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Prognostic indexes in primary dilated cardiomyopathy]. 234 26

We studied blood flow-promoting therapies after cardiac arrest in 18 dogs. Our model consisted of ventricular fibrillation (no blood flow) lasting 12.5 minutes, controlled reperfusion with cardiopulmonary bypass and defibrillation within 5 minutes, controlled intermittent positive-pressure ventilation to 20 hours, and intensive care to 96 hours. Group I (control, n = 6) dogs were reperfused under conditions of normotension (mean arterial blood pressure 100 mm Hg) and normal hematocrit (greater than or equal to 35%). Group II (n = 6) and III (n = 6) dogs were treated with norepinephrine at the beginning of reperfusion to induce hypertension for 4 hours. In addition, group III dogs received hypervolemic hemodilution to a hematocrit of 20% using dextran 40. There were no differences in the time to recovery of electroencephalographic activity among groups. All six group I dogs remained severely disabled; in groups II and III combined, six of the 12 dogs achieved good outcome (p less than 0.01). Some regional histopathologic damage scores at 96 hours were better in groups II and/or III than in group I (neocortex: p less than 0.05 group II different from group I; hippocampus: p less than 0.01 both groups II and III different from group I). Total histopathologic damage scores were similar among the groups. A hypertensive bout with a peak mean arterial blood pressure of greater than or equal to 200 mm Hg beginning 1-5 minutes after the start of reperfusion was correlated with good outcome (p less than 0.01). Our results support the use of an initial bout of severe hypertension, but not the use of delayed hemodilution.
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PMID:Hypertension with or without hemodilution after cardiac arrest in dogs. 238 98

The relationship between diuretic therapy and possible increased risk of coronary heart disease (CHD), especially sudden death, is controversial. The initial report from the Multiple Risk Factor Intervention Trial (MRFIT) raised the possibility that the increased CHD mortality observed in a subset of special intervention men with hypertension and certain electrocardiographic abnormalities on their baseline examination might be an unexpected adverse effect of diuretic therapy. Subsequent reports from the MRFIT have revealed a stronger association of CHD mortality to hydrochlorothiazide than to chlorthalidone. There was no consistent relationship of CHD mortality to the dose of either drug, to the most recent serum potassium level, or to the presence of ventricular premature beats. Unfavorable trends of the same magnitude were also seen among similar white men in the Hypertension Detection and Follow-up Program and in the Oslo hypertension trial, although the sample sizes in these two studies were too small to yield clearcut conclusions. Clinical studies have shown an increased risk of CHD death among hypertensive men with left ventricular hypertrophy. Such men are also noted to have a higher frequency of ventricular premature beats, even in the absence of diuretic therapy. Other studies have shown that diuretic-induced hypokalemia is accentuated in the presence of epinephrine and that low potassium levels decrease the threshold for ventricular fibrillation. Thus, although the evidence is still incomplete, it is possible that the excess CHD mortality among MRFIT special intervention men with electrocardiographic abnormalities may have been caused by a combination of increased left ventricular mass in the presence of coronary atherosclerosis, and hypokalemia caused by good compliance with diuretic therapy and accentuated by stress-induced increases in circulating catecholamines. Given the very large population of patients receiving diuretic therapy, further evaluation of this possibility is important.
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PMID:Unexpected effects of treating hypertension in men with electrocardiographic abnormalities: a critical analysis. 241 86

Cicletanine is a new antihypertensive agent. In view of its various pharmacological properties and of the different factors involved in sudden death, cicletanine was tested on an ischaemia-reperfusion model in anaesthesized dogs. In these experiments myocardial reperfusion induced ventricular fibrillation in 87 p. 100 of the cases, where as only 20% of those animals who received cicletanine 20 mg/kg intravenously 15 minutes before the 30 minute coronary occlusion developed ventricular disorders (p less than 0.001 vs controls). Moreover, cicletanine showed good antiarrhythmic activity during occlusion (total number of arrhythmias: 73.0 +/- 23.15 in treated animals, as against 293.4 +/- 40.03 in controls; p less than 0.05). Thus, antihypertensive treatment with cicletanine may prevent some of the cardiovascular risks associated with arterial hypertension.
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PMID:[Effect of cicletanine on a sudden death model in dogs]. 251 57

In order to test the effect of arterial hypertension on cardiac electrical activity, isolated Langendorff perfused hearts from spontaneously hypertensive (SHR) and normotensive (WKY) rats were studied. The incidence of spontaneous ventricular arrhythmias occurring during the control perfusion was 0% (n = 28) in WKY, 31% in SHR (n = 29, p less than 0.01), 7% (n = 14) in 3-month-old SHR, and 53% in 14-month-old SHR (n = 15, p less than 0.05). The incidence of ventricular arrhythmias induced by programmed electrical stimulation (PES = stimulus train + two extrastimuli) was 18% in WKY (n = 28), 48% in SHR (n = 27, p less than 0.05), 29% (n = 14) in 3-month-old SHR, and 69% (n = 13) in 14-month-old SHR (p less than 0.05). The incidence of PES-induced irreversible ventricular fibrillation was 0% in WKY and in 3-month-old SHR (n = 42), whereas it was 38% (n = 13) in 14-month-old SHR (p less than 0.001). Myocardial norepinephrine was significantly reduced in SHR with respect to WKY, but no significant difference was observed between 3-month-old SHR and 14-month-old SHR. Thus, no correlation between myocardial norepinephrine and ventricular arrhythmias could be found. It was concluded that the duration of hypertension was the most important factor in the development of severe ventricular arrhythmias.
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PMID:Age-related increase in the incidence of ventricular arrhythmias in isolated hearts from spontaneously hypertensive rats. 253 53

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

A prospective study correlated coronary risk factors with new coronary events in 192 elderly men and 516 elderly women, mean age 82 +/- 8 years. Follow-up was 41 +/- 6 months (range 24-44). Coronary events (myocardial infarction, primary ventricular fibrillation, and sudden cardiac death) occurred in 64 of 192 men (33%) and in 149 of 516 women (29%), P not significant. Using univariate analysis, significant risk factors for coronary events were antecedent coronary artery disease, cigarette smoking, hypertension, diabetes mellitus, serum total cholesterol (TC) greater than or equal to 200 mg/dL and greater than or equal to 250 mg/dL, serum high-density lipoprotein cholesterol (HDL-C) less than 35 mg/dL, and serum TC/HDL-C greater than or equal to 6.5 in men and women, and obesity in women. Using multivariate analysis, significant risk factors for coronary events were age, antecedent coronary artery disease, cigarette smoking, hypertension, diabetes mellitus, and serum TC in men and women and serum HDL-C and serum triglycerides in women. Using univariate analysis, significant risk factors for coronary events in men and women with antecedent coronary artery disease were cigarette smoking, diabetes mellitus, serum TC greater than or equal to 250 mg/dL, and serum TC/HDL-C greater than or equal to 6.5. Using multivariate analysis, significant risk factors for coronary events in men and women with antecedent coronary artery disease were age, cigarette smoking, diabetes mellitus, serum TC, serum HDL-C, and serum triglycerides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:41-month follow-up of risk factors correlated with new coronary events in 708 elderly patients. 271 56

Between January 1980 and December 1986, 2573 patients underwent simple first time coronary artery bypass grafting, of whom 73 (65 males and 8 females) aged 34-69 years (mean 51.3 yrs) had repeat bypass grafts at Wythenshawe Hospital, Manchester. Of these 73 patients, 15 had a previous myocardial infarction, 5 hyperlipidaemia, 4 systemic hypertension, and 12 had a strong family history of ischemic heart disease. There was an overall deterioration of left ventricular function at the time of reoperation. The interval between the two operations was 5-131 months (mean 34.2 mths); recurrence of angina occurred earlier (mean 18.4 mths). Vessels grafted at the first operation were LAD (59), RCA (46), circumflex (41) and diagonal (13). The corresponding data at reoperation were LAD (55), RCA (46), circumflex (28) and diagonal (10). Blocked grafts were seen in 67 patients and new lesions noticed in 29. Reoperation was done using saphenous vein (129), internal mammary artery (5), arm veins (2) and tubular Gortex grafts (2). One patient had concurrent excision of a left ventricular aneurysm. Coronary anastomoses were performed with elective ventricular fibrillation (47) or cardioplegic arrest (91). Aortic cross clamp time varied from 0-92 minutes. Seven patients required intra-aortic balloon support. These patients died in the first 30 days, an operative mortality rate of 4.1%, and two 18 months after surgery. Sixty-eight percent of patients seen at 1 year were totally symptom free. We conclude that reoperation for coronary artery disease can be done with a low mortality and good immediate relief of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Re-operation for recurrent coronary artery and graft disease. A review of 73 patients in a group of 2573 consecutive first operations. 278 23

In an attempt to identify the factors that influence survival after heterotopic heart transplantation, 42 consecutive recipients of heterotopic heart transplant were reviewed. Preoperative pulmonary artery pressures, pulmonary vascular resistance, and donor age significantly differed between hospital survivors and nonsurvivors. Postoperative survival analysis between pairs of groups of patients divided by each of these variables disclosed a significant difference, which confirmed the effects of these variables on survival. Evolution of pulmonary hemodynamics was compared between patients with preoperative pulmonary artery diastolic pressure greater than 25 mm Hg (pulmonary hypertension; n = 22) or less than 25 mm Hg (nonpulmonary hypertension; n = 20). Despite marked differences in preoperative pulmonary hemodynamics, pulmonary artery pressures were dramatically reduced immediately after transplantation, and pulmonary vascular resistance diminished to upper normal limits at 10 days when there were no longer differences in pulmonary vascular resistance between the two groups. Immediate deaths were related to left ventricular failure, and the incidence was similar between the groups. Despite such normalization of pulmonary hemodynamics, patients with preoperative pulmonary hypertension experienced more frequent ventricular fibrillation, required longer respiratory support, and developed lethal pulmonary or systemic infection, which resulted in a 32% (7/22) hospital survival rate compared with 90% (18/20) in patients without pulmonary hypertension. Despite the dramatic improvement in pulmonary hemodynamics, heterotopic heart failed to demonstrate the expected advantages because of frequent pulmonary complications and infection, which resulted in failure to improve the prognosis of patients with preoperative pulmonary hypertension.
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PMID:Factors affecting survival after heterotopic heart transplantation. 281 23


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