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

Postoperative mortality, infarction, and need for inotropic support are reportedly increased following myocardial revascularization in "high-risk" patients. We believe these complications result from inadequate protection of the compromised myocardium and should not occur with greater frequency in "high-risk" than "Low-risk" patients if the heart is optimally protected during the entire course of the operative procedure. Results following revascularization in 50 consecutive "low-risk" and 50 consecutive "high-risk" patients were analyzed. One or more of the followin factors were present in the "high-risk" group: ventricular dysfunction--ejection fraction less than 0.4, preinfarction angina, evolving infarction, recent infarction (less than 2 weeks), and refractory ventricular tachyarrhythmia. The following principles were used in all patients to minimize ischemic injury: 1) avoidance of pre-bypass hypo- or hypertension, 2) limitation of ischemic arrest to less than 12 minutes, 3) avoidance of ventricular fibrillation, and 4) prolongation of total bypass as necessary to repay the myocardial oxygen debt. Postoperative inotropic support was required in 10% of "high" and 10% of "low-risk" patients, new postoperative infarction developed in 10% of "high" vs. 10% "low-risk" patients; death occurred in 2% of "high" vs. 4% "low-risk" patients. These results are comparable and indicate that optimum myocardial protection allows safe revascularization in the "high-risk" patient.
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PMID:Coronary revascularization in "high" versus "low-risk" patients: The role of myocardial protection. 116 57

It is recognized that postoperative mortality, infarction and the need for inotropic support are increased following myocardial revascularization in highrisk patients. Operations were carried out in 57 such patients in whom one or more of the following factors were present: ventricular dysfunction-ejection fraction less than 0.4 (17), unstable (8) or preinfarction angina (29), evolving infarction (8), recent infarction (less than two weeks before) (5) and refractory ventricular tachyarrhythmia (4). Combined risk factors were present in nine patients. The following principles were utilized to minimize ischemic injury: (1) avoidance of prebypass hypertension and hypotension, (2) avoidance of extreme hemodilution, (3) avoidance of ventricular fibrillation, (4) maintenance of beating empty heart, when possible, (5) the limiting of ischemic periods to less than 12 minutes (hypothermia 32 degrees C) and (6) repaying myocardial oxygen debt with total (vented) bypass, when necessary. The following results were obtained: inotropic support was required in five patients (9 percent), "new" postoperative infarction occurred in five patients (9 percent) and one patient died (2 percent). These results are comparable to those reported in good-risk patients, and indicate that optimal myocardial protection will allow safe revascularization in a high-risk patient.
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PMID:Myocardial revascularization in high-risk coronary patients. 126 12

To evaluate the association between left ventricular false tendon (LVFT) and ventricular arrhythmias in acute myocardial infarction (MI) on the 1-st day of acute MI 71 patients were examined by 24-hour ECG-monitoring and M-mode, two-dimensional, Doppler echocardiography. LVFT was detected in 30 patients (42.3%). The frequency of left ventricular fibrillation, the number of patients with multiform ectopic ventricular beats (EVB), the number of single and pair EVB and runs of ventricular tachycardia were greater in group of patients with LVFT. 37 patients had Lown grades 1-2 (A) of arrhythmias, 34 patients had grades 3-5 (B). LVFT was revealed in four patients in group A (10.8%) and in 27 patients in group B (76.5%, p < 0.001). There were no significant differences between groups in left ventricular asynergy area and wall motion score, left and right ventricular, left atrium dimensions, left ventricular contractility indices, left ventricular walls thickness, frequency of mitral regurgitation. Multifactor analysis has shown significant relationship between Lown's class value and LVFT (p < 0.0001), Lown's class and arterial hypertension (p = 0.0376). Other 17 clinical factors were not connected with Lown's class value. Thus, LVFT was associated with severe ventricular arrhythmias in patients with AMI. This fact can be used as a predictor of these disturbances.
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PMID:Relationship between ventricular arrhythmias and left ventricular false tendons in acute myocardial infarction. 129 Jun 56

Congestive heart failure (CHF) is a common manifestation of hypertension, coronary artery disease, and dilated cardiomyopathy. The Framingham study showed that the incidence of CHF increases twofold with each decade of age. The presence of CHF increases the age-adjusted death rate 5.5-fold for women and 8-fold for men, and it increases the sudden death rate 5.5-fold in both men and women. Ventricular arrhythmias are a common accompaniment of CHF. Ambient ventricular premature complexes occur in most of these patients, and nearly one half of all CHF patients will have nonsustained ventricular tachycardia on a 24-h ambulatory electrocardiographic (Holter) recording. In addition, low left ventricular ejection fraction (LVEF) predicts inducible sustained ventricular tachycardia on electrophysiologic study. One-year mortality increases with worsening New York Heart Association (NYHA) Functional Class and decreasing LVEF. As the overall yearly mortality increases, the proportion of patients who die of arrhythmias decreases. The precise mechanism of death is frequently difficult to assess. Nonarrhythmic causes of death include CHF, shock, electromechanical dissociation, and myocardial rupture. Arrhythmic causes are most commonly due to ventricular tachycardia/ventricular fibrillation. Bradycardic events (asystole or heart block) are usually associated with progressively worsening CHF. Noncardiac causes that may confuse classification include pulmonary embolus and cerebrovascular accident. Because many patients have ischemic heart disease as the etiology of the CHF, a recurrent ischemic event can likewise make classification difficult. Overall, approximately one half of all deaths in CHF are arrhythmic and one half are nonarrhythmic.
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PMID:Clinical significance and management of arrhythmias in the heart failure patient. 139 10

Treatment with deoxycorticosterone acetate (DOCA) and salt for 12 weeks consistently induced hypertension in rats. Groups of treated rats and age-matched normotensive controls were killed 2 and 14 weeks after stopping the treatment. Two weeks after treatment with the corticoid, all the treated rats had left ventricular hypertrophy. Fourteen weeks after treatment the spontaneous regression of the hypertension was very variable, giving a wide range of ratios of left ventricular to body weight. The hearts were Langendorff-perfused and subjected to occlusion of the left coronary artery for 10 minutes at 37 degrees C. During reperfusion for 5 minutes, the severity of ventricular tachycardia and ventricular fibrillation was assessed. Two weeks after treatment, the incidence and duration of ventricular fibrillation were significantly greater in the treated hearts than in normal hearts. Fourteen weeks after treatment, the hearts with a ratio of left ventricular to body weight greater than 2.40 mg/g displayed a greater incidence of sustained ventricular fibrillation than controls and the median duration of ventricular fibrillation in this group was high. Conversely, the incidence of sustained ventricular fibrillation was lower in the treated group in which regression of the ratio of left ventricular to body weight was less than 2.40 mg/g; and the median duration of ventricular fibrillation was also reduced after regression of the left ventricular hypertrophy. This study provides evidence that regression of left ventricular hypertrophy may confer a reduced susceptibility to arrhythmias.
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PMID:Regression of left ventricular hypertrophy and susceptibility to reperfusion-induced arrhythmias after DOCA-salt hypertension in the rat. 147 92

Neomammalian and paleomammalian (limbic) brain structures control different behaviors and the autonomic support specific to each. Both neural systems are involved in cardiovascular disorders. Our previous studies showed that bilateral cryoblockade of a neomammalian structure (the frontal lobes) reduces blood pressure elevations in experimental hypertension and prevents lethal arrhythmogenesis in experimental myocardial infarction. Other studies showed that bilateral lesions in a paleomammalian structure (amygdala) also reduce the blood pressure elevations. Thus, we hypothesized that cryoblockade of the amygdala would prevent lethal arrhythmogenesis. We found that cooling of cryoprobes implanted bilaterally in the amygdala prevented ventricular fibrillation in five of eight pigs during a 20-minute period of reversible myocardial ischemia, whereas cryoblockade in structures surrounding the amygdala (five pigs), unilateral cryoblockade in the amygdala (two pigs), or sham operations (three pigs) did not prevent ventricular fibrillation (p less than 0.003). In two of the five pigs with amygdaloid blockade, the cooling was reversed at 20 minutes while the coronary occlusion continued (24 hours), and still ventricular fibrillation did not occur. In all other cases, ischemia was reversed at 20 minutes so that the heart could recover; this enabled histochemical documentation that the heart was normal at the time(s) ischemia was induced, and it allowed within-subject control experiments. Amygdaloid cryoblockade produced a small but significant increase in heart rate (10 beats per minute) without a change in blood pressure. We conclude that the paleomammalian brain, like its neomammalian counterpart, mediates brain effects on fatal arrhythmogenesis.
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PMID:Cryoblockade in limbic brain (amygdala) prevents or delays ventricular fibrillation after coronary artery occlusion in psychologically stressed pigs. 153 95

The pheochromocytoma syndrome, caused by an abnormal secretion of catecholamines, is a rare pathology responsible for 0.1-2% cases of hypertension in the overall population considered. Although in the past we deemed the pheochromocytoma could cause prevalently the typical syndrome characterized by paroxysmal hypertensive crises, now we think that the usual clinical presentation is a continue or subcontinue hypertensive state (65%). In this paper the authors refer the clinical experience acquired in 25 years in the General and Cardiovascular Institute of the University of Milan (head: Prof. Ugo Ruberti), analyzing epidemiological aspects and pathogenesis of pheochromocytoma, with particular care to diagnostic methodologies and referring the therapeutic choices. From 1965 until today 40 patients have been surgically treated for pheochromocytoma mono or bilateral. 43 operations have been done, carrying out 46 adrenalectomy. Two complication must be referred: an ictus cerebri consequent upon an hypertensive crisis and one death caused by intraoperative ventricular fibrillation. Normalization of arterial pressure has been obtained in all patients.
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PMID:[The clinical picture and surgery of pheochromocytomas. Our experience over 25 years]. 155 46

Coronary artery disease is the most serious complication of hypertension; therefore, the treatment of hypertension should be directed toward reducing the mortality from this disease. Since the majority of deaths occurring in post-myocardial infarction patients and hypertensive patients are sudden, the key objective is coronary artery disease treatment that will reduce the risk of sudden death. Several pharmacological interventions have been tested to determine whether they reduce the risk of sudden death. So far, only treatment with beta-adrenoceptor antagonists has been proven effective. Since most sudden cardiac deaths are due to ventricular fibrillation, an antifibrillatory effect on beta-adrenoceptor blockade has been invoked and demonstrated in clinical as well as animal experimental studies. Apart from an antifibrillatory effect, other effects of beta-blockade may also be involved. In the present review, different effects of beta-blockers that may contribute to the observed beneficial effects are discussed. The reduction in the risk of sudden death during active beta-adrenoceptor blockade reported in clinical studies is probably related to the summation of different effects, since cardiovascular drugs with a more limited mode of action (i.e., pure anti-ischemic effect or pure antiarrhythmic effect) have not shown similar impressive results.
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PMID:Prevention of sudden death using beta-blockers. Review of possible contributory actions. 168 8

We report on two patients, treated with indapamide for mild hypertension, who developed life-threatening ventricular arrhythmias. The former showed severe hypokalemia, QT interval prolongation and "torsade de pointes": the latter, who suffered from ischemic heart disease, had slightly decreased serum potassium and ventricular fibrillation. In both cases no other cause accounting for hypokalemia and ventricular arrhythmia was found. Therefore we stress that serum potassium and ECG must be carefully monitored during indapamide therapy, mainly in patients with cardiac disease.
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PMID:[Severe ventricular arrhythmia secondary to indapamide-induced hypopotassemia]. 170 75

Hypertension is associated with myocardial hypertrophy as well as increased adrenergic responsiveness, both of which can predispose to malignant ventricular arrhythmias. This study was designed to test the effects of subpressor doses of epinephrine (0.15 and 0.3 micrograms/kg/min x 30 min) on vulnerability to ventricular arrhythmia in normotensive and perinephritic hypertensive dogs. Two groups of 6 dogs each were chronically instrumented with aortic catheters to measure mean arterial pressure and bipolar pacing catheters in the apex of the right ventricle to measure repetitive extrasystole threshold, an index of vulnerability to ventricular fibrillation. In the normotensive dogs, the low dose of epinephrine (0.15 micrograms/kg/min IV) had no significant effects on mean arterial pressure, heart rate of repetitive extrasystole threshold. However, in the hypertensive dogs, the same dose caused a significant 39% increase in heart rate (p less than 0.05) and 41% decrease in repetitive extrasystole threshold (p less than 0.05). These findings suggest that electrophysiological vulnerability of the myocardium caused by epinephrine infusion is enhanced in the hypertensive animal.
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PMID:Decrease in repetitive extrasystole threshold during epinephrine infusion is enhanced in conscious dogs with perinephritic hypertension. 171 13


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