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

The authors report a case of pheochromocytoma recognized during surgery, at the manipulation of the tumor resulting in severe arterial hypertension, arrhythmia and a final unresponsive ventricular fibrillation. The anatomopathological examination confirmed the diagnosis of the pheochromocytoma in ectopic localization.
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PMID:[Hypertensive episode and arrhythmia with fatal outcome caused by pheochromocytoma discovered peroperatively]. 799 49

To elucidate the incidence and clinical significance of ventricular late potentials (LP) and reduced heart rate variability (HRV) in primary and secondary heart muscle disease, 157 patients with dilated cardiomyopathy (DCM, n = 19), chronic myocarditis (MC, n = 50), hypertrophic cardiomyopathy (HCM, n = 27) and systemic hypertension (HT, n = 61) were studied. LP measured by the signal averaging technique were found in 24% of the total study group--47% of the patients with DCM, 28% with MC, 29% with HCM and 10% with HT. Complex ventricular arrhythmias were detected during Holter monitoring in 56% of patients with DCM, in 41% with MC, in 21% with HT and in 16% with HCM. An electrophysiological study was performed in a total of 75 patients. Non-sustained or sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) were inducible during programmed ventricular stimulation in 32% of patients with MC, in 30% with HT, in 20% with DCM and in 17% with HCM. The total duration of the signal-averaged, filtered QRS complex was the only independent predictive factor for severe arrhythmic events and sudden cardiac death. HRV measured in 39 patients were most reduced in patients with DCM (RR interval standard deviation (HRV-SD) 39 +/- 23 ms), followed by 44 +/- 16 ms in patients with HCM, 45 +/- 28 ms in patients with HCM and 67 +/- 51 ms in patients with HT. A significant reduction in the HRV-SD below 30 ms was recorded in 24% of patients measured.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late potentials and heart rate variability in heart muscle disease. 799 67

Amrinone and dobutamine compare favorably in the treatment of chronic congestive heart failure. There is increasing evidence that amrinone alone or in combination with a catecholamine may be used with considerable success in treating patients who are difficult to wean from cardiopulmonary bypass or who have a low cardiac output syndrome after coronary artery bypass grafting surgery. Amrinone increases intramyocardial cyclic adenosine monophosphate and exerts positive inotropic activity in addition to being a potent vasodilator. It may also improve diastolic function by increasing sarcoplasmic reticulum reuptake of calcium during diastole. It has been administered to patients prior to weaning from cardiopulmonary bypass and has improved hemodynamics and oxygen transport. When compared with dobutamine as primary treatment for depressed myocardial function in patients being weaned from cardiopulmonary bypass after coronary artery bypass grafting surgery, it was more effective in achieving primary treatment objectives. Patients given dobutamine had a higher incidence of myocardial infarction, ventricular fibrillation, supraventricular tachyarrhythmias, sinus tachycardia, and hypertension compared to those given amrinone. It is concluded that amrinone compares favorably with dobutamine and may even be superior when used as primary treatment for treating myocardial depression in patients having coronary artery surgery supported by cardiopulmonary bypass.
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PMID:The role of amrinone in treating heart failure during and after coronary artery surgery supported by cardiopulmonary bypass. 806 35

The effect of angiotensin II on myocardial blood flow and acid-base status during cardiopulmonary resuscitation (CPR) was assessed. Fourteen pigs were allocated randomly to receive either 0.9% saline (n = 7) or 0.05 mg/kg angiotensin II (n = 7) after 4 min of ventricular fibrillation and 3 min of open-chest CPR. Total myocardial blood flow (measured with radiolabeled microspheres) before, 90 s, and 5 min following drug administration was 74 +/- 18, 62 +/- 12, and 54 +/- 11 mL.min-1 x 100g-1 (mean +/- SD) in the control, and 72 +/- 17, 125 +/- 25, and 74 +/- 20 mL.min-1 x 100 g-1 in the angiotensin II group (P < 0.001 at 90 s and P < 0.05 at 5 min). The PCO2 of coronary venous blood at 90 s after drug administration was 82 +/- 8 mm Hg in the control group as compared to 47 +/- 9 mm Hg in the angiotensin II group (P < 0.001). Only three of the seven control group animals could be resuscitated successfully, whereas all of the angiotensin II-treated pigs survived the 1-h observation period (P < 0.05), during which neither arterial hypertension nor bradycardia was observed. Angiotensin II was associated with an improvement of myocardial blood flow during CPR and short-term resuscitation success. The increase in myocardial perfusion is associated with a lower coronary venous PCO2 and a higher coronary venous pH. The authors conclude that angiotensin II administration facilitated cardiopulmonary resuscitation.
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PMID:Effect of angiotensin II on myocardial blood flow and acid-base status in a pig model of cardiopulmonary resuscitation. 845 55

We examined whether partial coronary sinus obstruction affects the latency of the early ventricular fibrillation (VF) of acute ischemia. During baseline trials 15 of 19 open-chest dogs fibrillated repeatedly and predictably within 2 to 5 minutes (251.6 +/- 64 seconds) after reversible, double coronary artery occlusion without developing profound hemodynamic deterioration. The effect of partial coronary sinus obstruction sufficient to increase coronary sinus pressure to 40 mm Hg could be adequately tested in 11 dogs. Coronary sinus obstruction consistently prevented VF in five dogs, significantly prolonged the VF latency in three (p < 0.01 to p < 0.001), and had no clear effect in another three. The overall effect was significant at the p < 0.01 level. VF latency prolongation/prevention was also positively correlated to the residual coronary sinus pressure at the time of VF (r = 0.76; p < 0.008), as well as the baseline VF latency (r = 0.75; (p < 0.008). The protective effect of coronary venous hypertension most likely reflects preservation of adequate extracellular fluid in the ischemic region after the perfusion arrest. This extracellular fluid may constitute a key component in the prevention of early ischemic arrhythmias by preserving interstitial hydraulic continuity and tissue homogeneity through enhanced dilution and diffusion of solutes.
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PMID:Protective effect of coronary sinus obstruction from primary ischemia-induced ventricular fibrillation in the dog. 846 71

Digoxin therapy has been suggested to increase mortality risk in survivors of acute myocardial infarction. Since digoxin is a drug with a narrow therapeutic/toxic ratio, we raised the hypothesis that the association between digoxin and post myocardial infarction mortality may have a dose-dependent relationship. The purpose of this study was to evaluate this hypothesis. We retrospectively analyzed data from 1731 survivors of acute myocardial infarction. At the time of hospital discharge, 175 patients (10%) were taking digoxin. The exact dosage of digoxin was ascertained in 153 (87%) patients. Patients were divided into two groups based on the weekly dosage of digoxin at hospital discharge: The first group included 41 patients who were treated with a low dose (< or = 1.5 mg per week, usually 0.125 mg daily). The second group included 112 patients treated with a full dose (> 1.5 mg per week, usually 0.25 mg daily). Both groups were comparable with regard to mean age, gender, history of prior myocardial infarction, diabetes mellitus, hypertension, and prior angina. There were no significant differences in the incidence of in-hospital complications, such as heart failure, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, and postinfarction angina. One year mortality was significantly higher among patients treated with a full dose [19 of 112 (17%)] than patients treated with a low dose of digoxin [1 of 41 (2%); p < 0.02] Multivariate analysis performed by the Cox proportional hazards model identified treatment with a full dose of digoxin as an independent determinant associated with increased death during the first year after myocardial infarction (hazard ratio 10.7; 95% confidence interval 1.4-80.5). Thus, mortality among myocardial infarction survivors treated with digoxin was related to a full-dose therapy. Patients treated with a low dose experienced a low mortality rate. Our findings raise concern that digoxin may exert a dose-dependent deleterious effect upon the survival of patients recovering from acute myocardial infarction.
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PMID:Digoxin and increased mortality among patients recovering from acute myocardial infarction: importance of digoxin dose. The SPRINT Study Group. 857 56

In 1961, in Pittsburgh, PA, "cerebral" was added to the cardiopulmonary resuscitation system (CPR --> CPCR). Cerebral recovery is dependent on arrest and cardiopulmonary resuscitation times, and numerous factors related to basic, advanced, and prolonged life support. Postischemic-anoxic encephalopathy (the cerebral postresuscitation disease or syndrome) is complex and multifactorial. The prevention or mitigation of this syndrome requires that there be development and trials of special, multifaceted, combination treatments. The selection of therapies to mitigate the postresuscitation syndrome should continue to be based on mechanistic rationale. Therapy based on a single mechanism, however, is unlikely to be maximally effective. For logistic reasons, the limit for neurologic recovery after 5 mins of arrest must be extended to achieve functionally and histologically normal human brains after 10 to 20 mins of circulatory arrest. This goal has been approached, but not quite reached. Treatment effects on process variables give clues, but long-term outcome evaluation is needed for documentation of efficacy and to improve clinical results. Goals have crystallized for clinically relevant cardiac arrest-intensive care outcome models in large animals. These studies are expensive, but essential, because positive treatment effects cannot always be confirmed in the rat forebrain ischemia model. Except for a still-elusive breakthrough effect, randomized clinical trials of CPCR are limited in their ability to statistically document the effectiveness of treatments found to be beneficial in controlled outcome models in large animals. Clinical studies of feasibility, side effects, and acceptability are essential. Hypertensive reperfusion overcomes multifocal no-reflow and improves outcome. Physical combination treatments, such as mild resuscitative (early postarrest) hypothermia (34 degrees C) plus cerebral blood flow promotion (e.g., with hypertension, hemodilution, and normocapnia), each having multiple beneficial effects, achieved complete functional and near-complete histologic recovery of the dog brain after 11 mins of normothermic, ventricular fibrillation cardiac arrest. Calcium entry blockers appear promising as a treatment for postischemic-anoxic encephalopathy. However, the majority of single or multiple drug treatments explored so far have failed to improve neurologic outcome. Assembling and evaluating combination treatments in further animal studies and determining clinical feasibility inside and outside hospitals are challenges for the near future. Treatments without permanent beneficial effects may at least extend the therapeutic window. All of these investigations will require coordinated efforts by multiple research groups, pursuing systematic, multilevel research--from cell cultures to rats, to large animals, and to clinical trials. There are still many gaps in our knowledge about optimizing extracerebral life support for cerebral outcome.
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PMID:Cerebral resuscitation from cardiac arrest: treatment potentials. 860 8

This study examined the early microvascular and neuronal consequences of cardiac arrest and resuscitation in piglets. We hypothesized that early morphological changes occur after cardiac arrest and reperfusion, and that these findings are partly caused by post-resuscitation hypertension. Three groups of normothermic piglets (37.5 degrees - 38.5 degrees C) were investigated: group 1, non-ischemic time controls; group 2, piglets undergoing 8 min of cardiac arrest by ventricular fibrillation, 6 min of cardiopulmonary resuscitation (CPR) and 4 h of reperfusion; and group 3, non-ischemic hypertensive controls, receiving 6 min of CPR after only 10 s of cardiac arrest followed by 4-h survival. Immediately following resuscitation, acute hypertension occurred with peak systolic pressure equal to 197 +/- 15 mm Hg usually lasting less than 10 min. In reacted vibratome sections, isolated foci of extravasated horseradish peroxidase were noted throughout the brain within surface cortical layers and around penetrating vessels in group 2. Stained plastic sections of leaky sites demonstrated variable degrees of tissue injury. While many sections were unremarkable except for luminal red blood cells and leukocytes, other specimens contained abnormal neurons, some appearing irreversibly injured. The number of vessels containing leukocytes was higher in group 2 than in controls (3.8 +/- 0.6% vs 1.4 +/- 0.4% of vessels, P < 0.05). Evidence for irreversible neuronal injury was only seen in group 2. Endothelial vacuolization was higher in groups 2 and 3 than in group 1 (P < 0.05). Ultrastructural examination of leaky sites identified mononuclear and polymorphonuclear leukocytes adhering to the endothelium of venules and capillaries only in group 2. The early appearance of luminal leukocytes in ischemic animals indicates that these cells may contribute to the genesis of ischemia reperfusion injury in this model. In both groups 2 and 3 endothelial cells demonstrated vacuolation and luminal discontinuities with evidence of perivascular astrocytic swelling. Widespread microvascular and neuronal damage is present as early as 4 h after cardiac arrest in infant piglets. Hypertension appears to play a role in the production of some of the endothelial changes.
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PMID:Early endothelial damage and leukocyte accumulation in piglet brains following cardiac arrest. 889 Oct 77

Left ventricular hypertrophy is associated with an increased risk of ventricular arrhythmia and multiple electrophysiologic abnormalities that normalize with regression of hypertrophy. For patients who have hypertension, treatment with angiotensin-converting enzyme (ACE) inhibitors produces regression of hypertrophy and a reduction in ventricular arrhythmia. It is unclear whether the reduction in ventricular arrhythmia associated with ACE inhibitor therapy is due to regression of hypertrophy alone, a direct antiarrhythmic effect of ACE inhibition, or both. We performed electrophysiologic studies in normal cats and cats with fixed left ventricular hypertrophy before and after acute intravenous administration of trandolopril. Trandolopril produced a small, consistent prolongation of monophasic action potential duration in normal and hypertrophied ventricles although this prolongation did not reach statistical significance. Trandolopril had no significant effect on effective refractory period, inducibility of arrhythmia, or ventricular fibrillation threshold in normal or hypertrophied ventricles. These data suggest that the reduction in arrhythmia associated with ACE inhibitors is not caused by a direct electrophysiologic effect but is more likely caused by regression of hypertrophy.
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PMID:Effect of an intravenous angiotensin-converting enzyme inhibitor on the electrophysiologic features of normal and hypertrophied feline ventricles. 889 73

Direct current electric shocks have been used to terminate atrial arrhythmias (cardioversion) in humans since the 1960s. The likelihood of successful cardioversion and maintenance of sinus rhythm is increased if the left atrium is not markedly enlarged and fibrotic, if there is no marked left atrial hypertension (e.g., mitral stenosis), and if the arrhythmia is not long-standing. To minimize the risk of thromboembolic phenomena, therapeutic anticoagulation should be established for at least 3 weeks before and for 4 weeks after cardioversion; coumadin is usually used for this purpose. A more recent approach uses transesophageal echocardiography to demonstrate the absence of thrombi in the left atrium and left atrial appendage. If no thrombi are evident, 48 hours of heparin anticoagulation may be adequate prior to cardioversion. Anticoagulation is still required after cardioversion. Quinidine and digitalis, singly or in combination, are frequently used to achieve and maintain sinus rhythm in association with cardioversion. For the procedure itself, traditional hand-held paddle electrodes or self-adhesive electrode pads may be used; the apex-anterior and anterior-posterior positions are equally effective. Gel couplants and firm pressure should always be used with hand-held paddles to reduce transthoracic impedance and maximize current flow. Electrodes should be widely separated to avoid shunting of current along the chest wall between electrodes. Generally, electrodes should be large in size; small "pediatric" electrodes should only be used in infants < 1 year of age (< 10 kg). Shocks should always be synchronized to the R wave to avoid the vulnerable period and the inadvertent induction of ventricular fibrillation. Initial shocks for atrial fibrillation should begin at 100 J; atrial flutter generally requires a smaller shock (initial shocks at 50 J). Effective anesthesia, not merely sedation, is required to achieve amnesia and avoid pain. Exciting new developments in defibrillation and cardioversion have occurred. It is now understood that excessive energy and current may induce cardiac damage, and recent studies suggest such damage may be mediated in part by free radicals. New shock waveforms, such as biphasic and multiphasic waveforms from multiple encircling electrodes, may be superior to the standard damped sinusoidal waveform.
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PMID:Transthoracic cardioversion of atrial fibrillation and flutter: standard techniques and new advances. 890 72


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