Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The focus of this article is hypokalemia, its electrophysiologic properties, and clinical arrhythmias. The effects of potassium on the electrophysiologic properties of the heart have been extensively studied and clearly are arrhythmogenic. Hypokalemia increases resting membrane potential and increases both the duration of the action potential and the duration of the refractory period, the latter to a greater degree than the former. This combination is conducive to the genesis of reentrant arrhythmias. Hypokalemia also increases threshold potential as well as automaticity, thus providing the context for automatic arrhythmias as well. Lastly, hypokalemia decreases conductivity, which also predisposes to arrhythmias of the reentrant type. The electrocardiographic criteria for hypokalemia include the presence of U waves greater than 1 mm and U waves larger than the T wave in the same lead (with associated ST-segment depression). Other criteria have been a T:U ratio of 1 or less and a U wave greater than 0.5 mm in electrocardiographic lead II or greater than 1.0 mm in lead V3. The relationship between hypokalemia and clinical arrhythmias has long been recognized. In 1949, Bellet et al reported extrasystoles with hypokalemic alkalosis that decreased with potassium administration. These observations were confirmed by several groups in the early 1950s. In 1953, Surawicz and Lepeschkin described a series of patients with hypokalemia and frequent junctional and ventricular premature beats; in all cases the arrhythmias disappeared with administration of potassium. These clinical observations were strengthened by the 1962 findings of Gettes et al, who employed microelectrode techniques to show that perfusion of low potassium solutions resulted in ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation. In more recent years, several studies have evaluated the relationship between potassium levels and arrhythmias in patients with and without hypertension who were receiving diuretic therapy. These studies have demonstrated that there is an increased incidence of ventricular arrhythmias associated with the hypokalemia induced by diuretic therapy, an observation with obvious clinical implications.
 ...
PMID:Hypokalemia and arrhythmias. 370 49

We investigated the ability of ouabain to produce lethal arrhythmias in rats with myocardial hypertrophy resulting from chronic renal hypertension. A gradual pressure overload was produced in female Wistar rats by left renal artery stenosis (two kidney, one clip, Goldblatt hypertension). Hypertension (systolic blood pressure greater than 150 mm Hg) developed within three weeks after clipping of the left renal artery and blood pressure continued to increase for the next five weeks. At ten weeks after the onset of hypertension animals were anesthetized with sodium pentobarbital (40 mg/kg) and artificially ventilated with room air while ECG was continually monitored and recorded. Continuous infusion of ouabain was maintained (0.7 mg/kg/min) through the inferior vena cava. Body weight and heart rate of control animals (C) was not significantly different from hypertensive (H) values, while systolic blood pressure in animals hypertensive for ten weeks was considerably greater (187 +/- 8.4 mm Hg) than their age-matched normotensive counterparts (123 +/- 6.0 mm Hg). Heart weight in hypertensive animals was elevated by 69% +/- 2.5 by time of study. Serological evaluation of both groups of animals revealed no significant differences in electrolytes and blood gases while significant differences were noted in glucose, BUN and creatinine. The average time to the first premature ventricular contraction was significantly shorter in H animals (3.5 +/- 0.2 min) when compared to C rats (6.0 +/- 0.2 min). The average time to ventricular tachycardia, ventricular fibrillation and death were also significantly shorter in H rats when compared to C animals (7.5 +/- 0.6 vs. 13.5 +/- 0.3; 13.5 +/- 0.5 vs. 21.0 +/- 0.5; 15.6 +/- 0.4 vs. 24.0 +/- 0.6 min). Thus, the hypertensive hypertrophied myocardium displays an increased propensity for lethal cardiac arrhythmias due to ouabain.
 ...
PMID:Renal hypertensive hypertrophy in the rat: a substrate for arrhythmogenicity. 371 25

The case of a 73-year-old man who developed acute thrombosis of the left subclavian artery during CPR is presented. The patient was known to have severe chronic obstructive lung disease, hypertension, coronary artery disease, and severe peripheral vascular disease. He was admitted with ventricular fibrillation. CPR was successful, and the ECG revealed acute extensive anterior and recurrent inferior wall myocardial infarctions. Soon after, acute occlusion of the left subclavian artery was diagnosed. Thrombectomy was performed and circulation was restored to the left upper limb. The patient died 12 hours later from severe bradycardia and asystole.
 ...
PMID:Acute thrombosis of subclavian artery during CPR. 382 17

The authors report a personal series of 60 cases of "torsade de pointe" (the largest series published to date) seen in the Cardiology department of Amiens Hospital over a period of 11 years. They review the essential features of this arrhythmia, which was well described by F. Dessertenne in 1966, but which is still sometimes confused with certain forms of ventricular tachycardia. "Torsade de pointe" is still a topical issue, as 25% of the cases in this series were seen over the last two years. These cases were classified into three groups according to their aetiology: severe bradycardia (21 cases), potassium depletion (16 cases), drug causes (23 cases). This arrhythmia was essentially associated with iatrogenic factors, in particular potassium depletion (41.6% of cases). The classical notion of predisposed patients was confirmed: elderly patients (mean age of 68 years), with cardiovascular disease in 70% of cases (i.e. heart failure or coronary insufficiency, hypertension) and with a marked female predominance (70% women). The ECG between episodes of "torsade de pointe" always revealed a prolonged QT interval which, in relation to the heart rate, was more marked in the patients with potassium depletion. During an attack, the average ventricular rate was 210/min (range: 170 to 290/min). 20% of cases subsequently developed ventricular fibrillation. The overall mortality was 16.6% (10 out of 60 cases), but there have been no deaths since 1977 due to the better understanding of this arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Torsades de pointe. Apropos of 60 cases]. 402 64

Phenylephrine, a strong alpha-adrenergic receptor-stimulating agent, was compared with adrenaline in 65 patients with out-of-hospital cardiac arrest, in a double-blind study. The resuscitation was performed by the physician-staffed Prehospital Emergency Care Unit of Helsinki University Central Hospital. The patients received either 1.0 mg of phenylephrine or 0.5 mg of adrenaline i.v. in the treatment of fine ventricular fibrillation, asystole or electromechanical dissociation. If two doses of either drug did not restore circulation, 0.5 mg of known 0.01% adrenaline was given i.v., maximally twice. In the adrenaline group, which consisted of 36 patients with a mean age of 61 years, 10 patients (28%) were successfully resuscitated. The phenylephrine group consisted of 29 patients with a mean age of 62 years. In this group nine patients (31%) were successfully resuscitated. The two groups were comparable regarding their apnoea-times, and there was no difference in the need for extra adrenaline between the groups. No adverse effects, such as hypertension or bradycardia, were noted in the patients treated with either adrenaline or phenylephrine, nor did the overall rate of successful resuscitation fall during the test period. It is concluded that phenylephrine seems as effective as adrenaline in the treatment of cardiac arrest, but further studies seem warranted.
 ...
PMID:Comparison of adrenaline and phenylephrine in out-of-hospital cardiopulmonary resuscitation. A double-blind study. 406 Oct 4

From 1973 to 1982, 253 patients--164 males and 89 females--underwent an operation for coarctation of the aorta in our clinic. Of the patients 72.3% presented with a circumscribed lesion and 58.5% with associated congenital cardiovascular defects. Resection with end-to-end anastomosis was performed in 138 patients (54.5%). Seventy-four patients (29.3%) had vascular graft prosthesis, 1.2% underwent the Clagett's operation, 9.1%, the indirect isthmoplasty and the rest (5.9%), the subclavian flap plastic. Ventricular fibrillation led to the intraoperative death of 3 infants with associated intracardiac and multiple somatic defects. The operative mortality was high in children under 15 months (13.2%), 1% in all the others taken together and 0% in all cases without concomitant lesions. Paraplegia occurred in only one patients (0.4%). One hundred twenty-eight patients were followed-up over a mean period of 3.6 years. The systolic and diastolic pressures decreased by a mean of 30 mmHg and 15 mmHg respectively. Eighty-seven patients (68%) had normal blood pressure at the time of examination. The rest (41 patients) had persistent postoperative hypertension necessitating medical management. The surgical technique elected did not influence the level and incidence of persistent postoperative hypertension, rather the level of the preoperative systolic right arm-to-leg pressure gradient (SPG) related closely to the incidence of persistent hypertension. Thirty patients (23.4%), among whom were 24 children under 10 years--some of them with preductal hypoplasia--presented with an SPG above 20 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Surgery of coarctation of the aorta: a nine-year review of 253 patients. 608 29

Calcium antagonists, of which the best known are verapamil, nifedipine and diltiazem, are a powerful group of cardioactive agents with a clinical spectrum of indications rather similar to those of beta-adrenoceptor blockade, including angina of effort, angina at rest, hypertension and supraventricular tachycardias (nifedipine is ineffective for the latter). In angina caused by coronary spasm, calcium antagonists are preferred to beta-blockade. Calcium antagonists have a basically different mode of action from beta-adrenoceptor blockade, although both ultimately act on the free cytoplasmic calcium ion concentration. Critical differences between the calcium antagonists are dependent on the individual properties of the calcium antagonists concerned. Different binding sites on the sarcolemma have been identified for nifedipine-like agents and verapamil, but with a different interaction with the nifedipine site. None of these sites might be relevant to the binding of calcium antagonists to the tissue of their therapeutic site of action (arterial smooth muscle for all; atrioventricular node for verapamil and diltiazem). As a group, calcium antagonists cause vascular dilation and do not cause bronchial constriction, in contrast to the beta-adrenoceptor blocking agents. In many patients, these diverse properties allow safe combination of calcium antagonists and beta-adrenoceptor blockers if due care is observed, especially in the case of nifedipine. The clinical differences between the effects of various calcium antagonists reflect: (i) the greater vasodilator capacity of nifedipine, so that at a given concentration the afterload effect dominates over possible effects on the nodal or myocardial tissue; (ii) the greater inhibition of vagal tone by nifedipine than by verapamil or diltiazem; and (iii) the greater inhibition of the atrioventricular node by verapamil and diltiazem. In angina of effort, calcium antagonists are now becoming the agents of first choice in some centers. Experimental use of calcium antagonists include the possible prevention of ventricular fibrillation, the inhibition of ischemic injury, the prevention of catecholamine mediated injury to the myocardium and decreased arterial calcinosis.
 ...
PMID:Calcium ions, drug action and the heart--with special reference to calcium antagonist drugs. 615 Nov 99

This review summarizes the available medical literature about plasma norepinephrine, which as been used as an indicator of sympathetic neural activity in clinical cardiology. Plasma norepinephrine levels are elevated myocardial infarction and congestive heart failure, and the norepinephrine concentration varies with severity of disease. Patients with ischemic heart disease at rest show essentially normal plasma norepinephrine, but no studies have assessed norepinephrine levels during spontaneously occurring typical angina pectoris. Plasma norepinephrine also is increased during hypertension occurring after coronary bypass surgery or repair of aortic coarctation. Propranolol increases plasma norepinephrine, and acute withdrawal of propranolol does not. Sodium restriction increases plasma norepinephrine in healthy persons, but no information is available about its effect on patients with congestive heart failure. Insufficient data are available to make strong inferences about sympathetic activity in cardiomyopathy, essential hypertension or pulmonary hypertension, and little or no information is available about plasma norepinephrine in ventricular fibrillation without myocardial infarction, the mitral valve prolapse syndrome, digoxin effect, syndromes associated with prolonged electrocardiographic Q-T interval and the hyperkinetic heart syndrome.
 ...
PMID:Plasma norepinephrine as an indicator of sympathetic neural activity in clinical cardiology. 617 Nov 57

Cardiac electrophysiologic alterations were evaluated 1 to 8 months after partial supracoronary aortic constriction in cats. This procedure induced left ventricular systolic hypertension and hypertrophy with marked connective tissue infiltration. In situ, premature ventricular complexes were observed during or after vagal slowing of sinus rate in 8 (26%) of the 31 experimental animals, while an additional 3 of the 31 developed ventricular fibrillation. No arrhythmias were recorded in 31 normal or 7 sham-operated cats. In vitro, 29% of the left ventricular preparations from cats with pressure overload and 5% from control cats showed spontaneous ectopic activity. During stimulation at cycle lengths of 800 to 1,000 ms, multiple site impalements of subendocardial muscle cells within fibrotic regions revealed heterogeneous electrical abnormalities. These included short action potential duration, low amplitude action potentials generated from low resting potentials, split upstrokes and electrically silent areas. Impalements in nonfibrotic areas of the left ventricle showed prolongation of muscle action potential duration. Long-term disturbances in cellular electrophysiologic properties may favor the development of arrhythmias and thereby contribute to sudden cardiac death in left ventricular hypertension and hypertrophy.
 ...
PMID:Electrophysiologic consequences of chronic experimentally induced left ventricular pressure overload. 619 60

During acute myocardial infarction an increase in arterial pressure is common in patients who were previously normotensive and, therefore, do not have left ventricular hypertrophy. However, the effect of hypertension on infarct size in the absence of hypertrophy is uncertain. Thus, 32 open chest dogs underwent a 2 hour occlusion of the mid-left anterior descending coronary artery followed by 3 hours of reperfusion. Immediately after occlusion, 14 dogs were randomized to a hypertension group (intravenous phenylephrine infusion starting 5 minutes after occlusion and terminating at the time of reperfusion, with heart rate kept constant by atrial pacing) and 18 dogs to a control group (equivalent volumes of saline solution intravenously). Twelve of the 32 dogs were excluded from analysis because they developed ventricular fibrillation during coronary occlusion or reperfusion. In the hypertension group (n = 10), the mean arterial pressure increased significantly within 10 minutes of coronary occlusion (146 +/- 7 versus 109 +/- 11 mm Hg in 10 control dogs, p less than 0.01) and was maintained approximately 40 mm Hg higher than in the control group (p less than 0.01) throughout the ischemic period. Heart rate was similar in the two groups throughout the experiment. After the dogs were sacrificed, the region normally supplied by the occluded artery (anatomic "region at risk") was identified by simultaneous perfusion of the aortic root and the coronary artery distal to the occlusion. The heart was sectioned transversely and stained with triphenyltetrazolium-chloride. The infarcted area and the anatomic risk area were determined by video planimetry.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Influence of acute arterial hypertension on myocardial infarct size in dogs without left ventricular hypertrophy. 623 49


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>