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

Factors related to long-term (post-discharge) outcome following successful resuscitation from pre-hospital ventricular fibrillation by a physician-manned mobile coronary care unit were studied. Between 1 January 1966 and 31 December 1987, 190 patients were resuscitated from pre-hospital ventricular fibrillation (158 male; mean age 56 years). The aetiology of ventricular fibrillation was acute myocardial infarction in 131 patients (69 per cent), ischaemic heart disease without infarction in 48 (25 per cent) and other or unknown in 11 (6 per cent). Predicted actuarial survival rates at 1, 2, 5, 10 and 20 years were 76 per cent, 66 per cent, 41 per cent, 27 per cent and 12 per cent respectively. Of 128 recorded deaths over 20 years, 85 per cent were cardiac and 48 per cent were defined as sudden death outside hospital. Factors significantly associated with increased long-term mortality (p less than 0.05), based on analysis of 10 year actuarial life tables using the Lee-Desu statistic were ventricular fibrillation due to ischaemic heart disease without infarction rather than acute myocardial infarction, a history of previous myocardial infarction, a history of hypertension, digoxin and diuretic therapy before ventricular fibrillation and digoxin as discharge medication, and failure to stop smoking after discharge from hospital by patients who had been smoking prior to ventricular fibrillation. In addition, Cox's regression analysis showed that patient age greater than or equal to 60 years was significantly associated with increased long-term mortality. On multivariate analysis, factors independently associated with increased long-term mortality were ventricular fibrillation occurring before 1977, previous myocardial infarction or hypertension and digoxin as discharge medication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term survival after resuscitation from ventricular fibrillation occurring before hospital admission. 175 73

To evaluate the effects of hypertension on cardiac hypertrophy, on myocardial structure, and on ventricular arrhythmias, 27 3-month-old spontaneously hypertensive rats were treated with enalapril (10 mg/kg) daily for 11 months and compared with 26 untreated control rats. Systolic arterial pressure was significantly decreased in treated rats, and at the end of the experiment, it was 199 +/- 3 mm Hg (treated) versus 237 +/- 3 mm Hg (controls) (p less than 0.001). At this time, spontaneous arrhythmias and induced arrhythmias either by programmed electrical stimulation (train of stimuli +1 or 2 extrastimuli) or by trains of eight stimuli at decreasing coupling intervals were observed in isolated heart preparations. Comparing enalapril-treated and control rats, spontaneous arrhythmias (9 of 27 versus 20 of 26, respectively; p less than 0.01), programmed stimulation-induced arrhythmias (3 of 26 versus 12 of 23, respectively; p less than 0.01), and trains of stimuli-induced arrhythmias (4 of 26 versus 14 of 19, respectively, p less than 0.001) were less frequent in the enalapril group. Left ventricular weight was decreased in treated rats by 18% (p less than 0.001). Enalapril administration diminished the fraction of myocardium occupied by foci of replacement fibrosis normally occurring in control rats by 59% (p less than 0.001). Finally, a significant correlation was found between left ventricular weight, the extent of myocardial fibrosis, and the occurrence of ventricular fibrillation. It was concluded that chronic treatment with enalapril, which resulted in attenuation of systemic arterial pressure by limiting cardiac hypertrophy and myocardial fibrosis, decreases the propensity of the heart of hypertensive rats to arrhythmogenesis.
Hypertension 1991 Aug
PMID:Enalapril prevents cardiac fibrosis and arrhythmias in hypertensive rats. 188 22

Sequences of ventricular fibrillation-defibrillation cause transient hypertension; we hypothesized that this "adrenergic overshoot" might be blunted by the functional antiadrenergic effect of the calcium channel blocking drug nisoldipine, with a potentially beneficial reduction in myocardial oxygen requirements. However, other calcium channel blocking drugs have been shown to reduce shock success for defibrillation, a deleterious effect. Thus the purposes of this study were to assess the effect of nisoldipine on the hemodynamic responses to the sequences of ventricular fibrillation-defibrillation, and its effect on the energy requirements for defibrillation. In 16 dogs we administered intravenous nisoldipine (1 microgram/kg bolus followed by an infusion of 0.075 to 0.50 microgram/kg/min) to lower mean blood pressure 10% and 20% below baseline. Ventricular fibrillation was induced electrically, and shocks of varying energy levels (30, 50, and 100 joules) were administered to determine defibrillation energy requirements. Heart rates and blood pressures were recorded up to 3 minutes after each shock to determine hemodynamic responses. Measurements were made before nisoldipine administration and again at the two levels of drug-induced blood pressure decline. We found that the usual systolic blood pressure "overshoot" after defibrillation (typically maximum at 15 to 30 seconds after shocks) was significantly blunted after nisoldipine administration (p less than 0.05). Heart rate slowing after defibrillation (a cholinergic response) was not affected. Nisoldipine did not alter shock success rates, which varied from 12 +/- 7%SE at 30 joules to 68 +/- 12% at 100 joules. Thus nisoldipine blunted the "adrenergic overshoot" of systolic blood pressure following defibrillation, a potentially beneficial effect, without altering the energy requirements for transthoracic defibrillation.
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PMID:Effect of nisoldipine on hemodynamic responses to defibrillation. 200 Jul 51

The effect of magnesium sulfate on ventricular refractoriness and its efficacy for torsade de pointes (TdP) were studied in nineteen dogs. After the administration of quinidine sulfate (30 mg/kg), TdP was induced by ventricular pacing in ten of 19 dogs (52.6%), polymorphic ventricular tachycardia in seven (36.8%), ventricular fibrillation in two (10.5%). Quinidine sulfate caused significant increases in QTc interval, ventricular effective refractory period (ERP) and dispersion of ERP(dERP), and decrease in ERP/QT. Magnesium sulfate significantly increased ERP (p less than 0.01), but it did not change QT interval, resulting in significant increasing of ERP/QT (0.41 +/- 0.05 to 0.61 +/- 0.05, p less than 0.01). It decreased dERP but not significantly. Magnesium sulfate prevented the induction of TdP in eight of 10 dogs (80.0%) (30 mg/kg in four and 60 mg/kg in four). In conclusion, magnesium sulfate has value as first aid therapy for drug-induced TdP. If patients have ischemic heart disease or hypertension, we recommend infusion of magnesium for the initial therapy of TdP.
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PMID:Effect of magnesium sulfate on ventricular refractoriness and its efficacy for torsade de pointes. 209 63

The authors performed a prospective study to correlate echocardiographic left ventricular hypertrophy (LVH) and silent ischemia (SI) detected by twenty-four-hour ambulatory electrocardiographic monitoring with new cardiac events in 355 patients, mean age eighty-two +/- eight years, with systemic hypertension or coronary artery disease (CAD). Cardiac events included myocardial infarction, primary ventricular fibrillation, or sudden cardiac death. Mean follow-up was thirty-one +/- seven months (range twelve to forty). Cardiac events occurred in 28 of 147 patients (19%) without LVH or SI (A), in 56 of 113 patients (50%) with LVH and no SI (B), in 16 of 29 patients (55%) with SI and no LVH (C), and in 52 of 66 patients (79%) with LVH and SI (D). Significant p values were p less than 0.001 comparing D with A, D with B, C with A, and B with A; and p less than 0.02 comparing D with C. These data indicate that echocardiographic LVH and SI detected by ambulatory electrocardiographic monitoring are independent risk factors for new cardiac events in elderly patients with systemic hypertension or CAD.
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PMID:Usefulness of echocardiographic left ventricular hypertrophy and silent ischemia in predicting new cardiac events in elderly patients with systemic hypertension or coronary artery disease. 213 98

Antihypertensive management reduces the incidence of congestive heart failure, malignant hypertension and stroke; however, the overall incidence of events due to ischemic heart disease was not influenced by antihypertensive treatment. One of the possible explanations might be some negative metabolic effects of antihypertensive drugs. Hypokalemia develops in 20 to 50% patients who receive a thiazide diuretic. An association between hypokalemia and malignant arrhythmias (including ventricular fibrillation), in acute myocardial infarction, has been observed. 24-hour ambulatory electrocardiographic monitoring demonstrated a higher frequency of ventricular ectopic beats in hypertensive patients taking thiazides. There is, however, no convincing evidence of a simple causative relation between ventricular extrasystoles and low concentrations of serum potassium. Hypertensives with left ventricular hypertrophy (ECG criteria) had significantly more premature ventricular contractions than patients with established hypertension without left ventricular hypertrophy or normotensive subjects. These data could provide an electrophysiologic substrate for the epidemiologic findings of increased morbidity and mortality in patients with left ventricular hypertrophy.
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PMID:The heart in hypertension and arrhythmias. 213 16

Important electrophysiological alterations that may predispose hearts to arrhythmias have been described for hypertrophied myocytes, and hypertrophy coupled with ischemia has been associated with an increased incidence of sudden death; however, an influence of hypertrophy on reperfusion arrhythmias has not been previously described. We hypothesized that reperfusion-associated arrhythmias would be potentiated by left ventricular hypertrophy. After induction of renovascular hypertension, 37 awake, unsedated dogs (17 with left ventricular hypertrophy and 20 without hypertrophy) underwent 15 minutes of coronary artery occlusion and reperfusion. All dogs were pretreated with lidocaine bolus injections and with lidocaine by continuous infusion during coronary occlusion and reperfusion. Reperfusion-associated ventricular fibrillation occurred in seven of 17 dogs with left ventricular hypertrophy versus one of 18 dogs without hypertrophy (p less than or equal to 0.05). The presence of hypertension was not significantly associated with an increased incidence of reflow ventricular arrhythmias. Neither QT interval nor area-at-risk was different between the dogs with and without reperfusion ventricular fibrillation; however, increased heart rate just before reperfusion did correlate with an increased incidence of ventricular fibrillation at reperfusion. Thus, 1) left ventricular hypertrophy was associated with a significantly increased incidence of reperfusion-induced ventricular fibrillation after 15 minutes of ischemia, 2) this increased incidence was independent of the presence of hypertension, and 3) lidocaine protected control and hypertrophied hearts against ventricular fibrillation during ischemia but was ineffective in protecting hypertrophied hearts against reperfusion-induced ventricular fibrillation.
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PMID:Potentiation of reperfusion-associated ventricular fibrillation by left ventricular hypertrophy. 214 98

Established hypertension is associated with enhanced susceptibility to life-threatening arrhythmias. However, little is known about the effects of the development of hypertension on the electro-physiological properties of the heart. To study this relationship, dogs were chronically instrumented for recording mean arterial pressure and conducting cardiac electrical testing during right ventricular pacing using an intracavitary bipolar catheter. In normotension, ventricular fibrillation threshold was determined under alpha-chloralose anesthesia, after which perinephritic hypertension was induced by wrapping one kidney in silk followed by contralateral nephrectomy. During serial testing of the same animals, ventricular fibrillation threshold was significantly increased early in the development of hypertension (2 to 3 weeks after renal wrapping), but found to be significantly reduced at 6 to 7 weeks after renal wrapping. The increase in ventricular fibrillation threshold was eliminated by cholinergic blockade.
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PMID:Changes in ventricular fibrillation threshold during the development of perinephritic hypertension. 214 66

The pattern of dying from immersion hyperthermia was documented in 8 dogs, 9 rhesus monkeys and 12 pigtail monkeys. Under light general anesthesia and spontaneous breathing, the animals were immersed into water of 45 degrees C, which was subsequently adjusted to control brain (parietal epidural) temperature at 42 +/- 0.5 degrees C. Transient initial hypertension, tachycardia, tachypnea and hypocarbia were followed by progressive hypotension with decreasing central venous pressure and pulmonary artery occlusion pressures (measured in three dogs only), bradycardia and bradypnea. Cardiac arrest occurred in the dogs after immersion of 288 +/- 66 min and more rapidly (P less than 0.02) in the rhesus monkeys (at 137 +/- 75 min) and pigtail monkeys (at 178 +/- 26 min). EEG silence occurred in the monkeys at MAP 40 mmHg and in the dogs at MAP 25 mmHg. Cardiac arrest occurred in form of sudden ventricular fibrillation (2/5 dogs, 2/9 rhesus monkeys, 3/12 pigtail monkeys), or later in electromechanical dissociation leading to electric asystole (3/5 dogs, 7/9 rhesus monkeys, 9/12 pigtail monkeys). The mean blood glucose levels decreased to less than 30 mg/dl (P less than 0.002), whereas hematocrit, serum osmolality, lactate and potassium levels increased. Necropsies revealed macroscopic petechial hemorrhages in all extracerebral organs, but not in the brain. There was no gross evidence of cerebral edema. Death seemed to be the result of primary cardiovascular failure leading to secondary (ischemic) cerebral failure (EEG silence) and apnea, which coincided with pulselessness.
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PMID:Hyperthermia-induced cardiac arrest in dogs and monkeys. 217 84

In 5,839 consecutive patients with acute myocardial infarction (AMI), hospitalized between July 1981 and July 1983 in 14 coronary care units in Israel, the incidence of primary ventricular fibrillation (VF) was 2.1%. Patients with primary VF resembled counterparts without VF in terms of age, gender, frequency of previous AMI and past cigarette smoking habits. The hospital course of patients with primary VF revealed increased incidence of primary atrial fibrillation and atrioventricular block. Increased serum levels of glutamic oxaloacetic transaminase and lactic dehydrogenase were noted among the patients with primary VF. In-hospital mortality rate was 18.8% in 122 patients with primary VF compared with 8.5% in 3,707 patients forming the reference group (p less than 0.01). Adjustment by age using logistic function yielded an estimate of 2.86 for relative mortality odds associated with primary VF, and further adjustment by gender, history of AMI, systemic hypertension, and by enzymatically estimated infarct size slightly reduced the estimated odds, at 2.52 (95% confidence interval, 1.42 to 4.46). Prognosis after discharge from the hospital was independent of primary VF. In conclusion, primary VF exerts an independent, significant effect on in-hospital mortality.
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PMID:Prognosis of acute myocardial infarction complicated by primary ventricular fibrillation. Principal Investigators of the SPRINT Study. 223 24


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