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

The interpretation of IE recorded in children has been hampered by a lack of agreement regarding normal values. We recorded IE in 158 children and young adults (ages, three days to 33 years) to define the various conduction intervals in normal and disease states. The HBP was recorded in 156 subjects. In 85 subjects with normal conduction indicated by surface ECG, including 19 subjects with normal hearts, there were no statistically significant age-related differences in internodal, A-V nodal, or His-Purkinje conduction intervals. Therapeutic levels of digitalis did not alter the conduction intervals. In 11 subjects with first degree A-V block and in five subjects with congenital complete A-V block, the site of block as determined by IE could not be predicted from the surface ECG. No abnormalities in conduction intervals were found in 18 subjects with right bundle branch block (surgically induced in 17 cases). Intracardiac electrography with recording of the HBP was found to be a safe, informative technique for electrophysiologic investigations in children and young adults.
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PMID:Intracardiac electrography in children and young adults. 4 75

Twelve chemical rhyzolisis (surgical instilation of 10 c.c. of 15% NaCl solution) of trigeminal nerve were performed in 11 patients with trigeminal neuralgia resistent to medical treatment. Before and at least in the first 30 minutes after instilation the following parameters were monitorized: electrocardiogram, electroencephalogram, intrarradial arterial pressure and venous central pressure. In 10 cases after a 2.8 +/- 2.4 seg. latency period the following arrhythmias appeared (in paragraphs number of cases): sinus bradicardia, sinoauricular block, sinus arrest, atrial-ventricular block and atrial pacemaker migration. During sinus arrest (8 episodes in 4 cases; mean duration 17.6 secs.) slow, high voltage waves appeared in the electroencephalographic tracings. Ventricular scapes were not seen at the end of the sinus pauses. In 6 cases after this slow arrhythmic phase the following arrhythmias were observed: ventricular premature beats, atrial premature beats, sinus tachycardia, bidirectional ventricular tachycardia, and nodal tachycardia. All cases exhibited an elevation of mean arterial pressure after instilation of the nerve which was preceded by a short period of hypertension in 4 occasions. Average and standard deviations changes of systolic, diastolic and mean blood pressure (mm of Hg), pulse (beats/minute) and central venous pressure (cms of H2O) during the procedure were 46.7 +/- 29.3, 23.0 +/- 13.3, 34.1 +/- 16.4, 25.8 +/- 16.2 and 6.6 +/- 5.8, respectively (p less than or equal to 0.001) in all changes but the last ones, less than or equal to 0.05). Physiopathologic considerations of this autonomic crises are done.
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PMID:[Cardiovascular manifestations of chemical rhysolisis of the trigeminal nerve]. 54 21

The electrophysiologic effects of hydralazine were evaluated in nine hypertensive patients with sinoatrial dysfunction. Intravenous hydralazine, 0.15 mg/kg, caused no significant reduction in arterial blood pressure. Yet this dose of hydralazine increased heart rate from 61.9 +/- 4.1 beats/min (mean +/- standard error of the mean) to 68.6 +/- 4.9 (P less than 0.001). Sinus nodal recovery time upon termination of atrial pacing shortened from 3,207 +/- 1,098 to 2,064 +/- 573 msec (P less than 0.05) and second escape cycles shortened as well (P less than 0.025). Acceleration of heart rate and abbreviation of recovery time did not closely correlate with change in blood pressure (r = 0.41 and 0.18, respectively). Junctional escape beats became more frequent and junctional escape time shortened from 2,525 +/- 692 to 1,705 +/- 382 msec (P less than 0.05). Sinoatrial conduction time tended to shorten, but a significant change was not observed. Atrial tachyarrhythmias did not occur and atrial refractoriness was unchanged. Thus, a minimal blood pressure response to hydralazine was associated with enhanced automaticity. Hydralazine merits clinical trial for treatment of sick sinus syndrome with concomitant hypertension.
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PMID:Electrophysiologic effects of hydralazine on sinoatrial function in patients with sick sinus node syndrome. 64 82

Twenty four cases with myocardial rupture among 259 patients with autopsy after death due to myocardial infarction, were compared with patients with acute myocardial infarction and death secondary to other causes. Myocardial rupture occured during the first 72 hours in 58% of the patients and all cases within the first five days. Two thirds of the patients were males and 46% were 70 years of age. There were 24 myocardial ruptures (9.5%). Previous history of arterial hypertension and un-remittent anginal pain were predisposing factors for rupture (p=0.05). Other previously reported bad prognostic factors such as persistent hipertension after acute infarction, severe exercise before infarction and history of Diabetes Mellitus were not statistically significant in this study. Ruptured myocardium was not influenced by a previous history of myocardial infarction, hospitalization delay in the C.C.U., administration of anticoagulants, digitalis or pressor amines. There was no significant difference among the groups compared in enzyme curves or magnitude of leucocytosis. Electromechanic dissociation, sinus bradycardia, nodal rhythm followed by idioventricular rhythm and asystole, were observed following myocardial rupture.
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PMID:[Rupture of the free wall of the heart as cause of death in acute myocardial infarct]. 66 44

Cardiovascular collapse associated with pneumoencephalography (PNE) has been reported but there has been no prospective study of its nature and cause. We have recorded prospectively the e.c.g. of 82 unselected patients, with no cardiovascular or metabolic disease, undergoing PNE under general anaesthesia. The frequency of arrhythmia following air injection was 60%; bradycardia 22%; ventricular ectopic beats 26%; nodal rhythm or sinus tachycardia 11%. Cardiovascular collapse occurred in three patients; two with "torsades de pointes" and one with bigeminy and q.r.s. block. Arrhythmia was more frequent in patients with a pituitary tumour and intracranial hypertension (91%). Eight postoperative control PNE examinations were uneventful. Three of four patients with frontal lobe tumours and four of seven with posterior fossa tumours exhibited arrhythmia.
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PMID:Cardiac arrhythmia induced by pneumoencephalography. 67 72

Heart block was noted in 60 (35 complete and 25 second-degree) of 410 patients with acute inferior wall myocardial infarction. This group with heart block was compared to a control group of 30 patients with acute inferior wall infarction without heart block. The incidences of prior myocardial infarction and hypertension, in addition to the highest level of serum creatine phosphokinase and a maximum degree of ST-segment elevation in the inferior leads, were all greater in patients with heart block, as compared to the controls. The incidences of various complications, including dizziness and syncope, transient hypotension, cardiogenic shock, and congestive heart failure, were also higher in the group with heart block, while sinus nodal distrubances and atrial arrhythmias occurred with equal frequency. The mortality in those with heart block was 28 percent compared to 13 percent for the control. It is concluded that patients with heart block complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis, a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker should be considered when specific indications are present and not routinely.
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PMID:Heart block complicating acute inferior wall myocardial infarction. 126 67

Fifteen cases of chronic heart block were studied. Eight of them could be designated as idiopathic or primary heart block; the others were associated with hypertension, diabetes and ischaemic heart disease, either singly or in various combinations. In six cases, the whole heart was available for histopathological study of the conduction system. In the other 9 cases, only a portion of the heart muscle was available for examination. A V nodal fibrosis extending upto the proximal bundle of His was seen in all the six whole heart autopsy materials. Fibrosis of the adjacent myocardium was seen in five cases. In three cases, conducting system fibrosis was associated with atherosclerotic (1 case) or diabetic changes (3 cases) of the intramural vessels. In the 9 partial autopsy studies, myocardial fibrosis was seen in two cases, diabetic microangiopathy in one and atherosclerotic changes in two including an old thrombus in one. Thus, diabetic microangiopathy was seen in total four cases. These changes may be responsible for the cardiomegaly and cardiac failure associated with conduction defects observed in diabetes. In the idiopathic group also, heart block could be considered as a significant facet of a primary myocardial degenerative process.
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PMID:Cardiac changes implicated in chronic heart block. 181 5

The four classes of first-line antihypertensive agents recommended in the 1988 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure are reviewed here. Particular consideration is given to the effects of these agents on heart rate, atrioventricular nodal conduction, and myocardial contractility in patients with other cardiovascular diseases. Diuretics and angiotensin-converting enzyme inhibitors have no significant direct effects on cardiac function. beta-Blockers inhibit catecholamine stimulation of the heart and may be particularly beneficial in treating patients with a history of myocardial infarction. Calcium channel blockers reduce blood pressure by dilating arterial resistance vessels. They are structurally heterogeneous and highly selective in their sites of action. As a consequence, cardiac effects can be minimized by selecting a calcium channel blocker with more potent peripheral vasodilatory effects. A new calcium channel blocker, isradipine, currently undergoing clinical trials, is highly selective for arterial smooth muscle and appears to be a safe and effective antihypertensive agent.
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PMID:Cardiac contractility and conduction: a comparison of antihypertensives. 197 5

Holter recordings of subjects apparently free from cardiovascular disease have demonstrated a moderate sinusal and nodal depression during sleep. This depression does not seem to be sufficient to create overt cardiovascular disorders in apparently healthy subjects, but it may aggravate or even reveal an underlying disorder of rhythm or conduction in elderly people or in patients taking drugs that potentiate its effects. In sleep apnea syndrome prolonged episodes of apnea may produce a paroxysmal, then permanent increase in pulmonary arterial pressure, which may lead to right heart failure. These episodes also increase the pre- and after-load and decrease myocardial contractility, thus facilitating the occurrence of left ventricular failure, potentiated by systemic arterial hypertension, overweight or even coronary disease, all conditions that are often present in these subjects. Arterial hypertension is so frequent in sleep apnea syndrome that some authors advocate a systematic search for the syndrome by Holter recordings before the hypertension is pronounced "essential". All studies confirm the existence of rhythm and conduction disorders directly related to apneic episodes. These disorders decrease or regress after a well-conducted treatment of the sleep apnea syndrome. They are mainly of the "hypokinetic" type, created by depression of sinus activity and conduction pathways. Their frequency, their severity and, in particular, the risk of sudden death they carry seem to have been overestimated, especially since no evidence has ever been produced of a potentially lethal rhythm disorder occurring during sleep apnea. Nevertheless, there is no certainty that these patients are not at risk of sudden death related to their sleep apnea syndrome.
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PMID:[Cardiovascular disorders during sleep]. 214 78

Ca2+ channel antagonists are agents that interact with the voltage-dependent Ca2+ channel in a highly specific way. The prototype agents of cardiovascular importance are verapamil, nifedipine, and diltiazem, in historical order of appearance. These agents all have different molecular structures and bind separately with receptor sites located in or near the calcium channel, at molecular sites still to be fully identified. There are probably three distinct receptor sites (V, N, D) which stand in relation to the "gate" of the long-acting "L" calcium channel. There is probably overlap among the receptor sites, especially between the V and D sites to explain their common properties. All three agents inhibit the voltage-dependent calcium channel in vascular smooth muscle and also myocardial slow calcium channels. The ratio of the arterial to the myocardial effect is an index of the arterial selectivity, generally held to be a desirable property because the negative inotropic effect is usually a liability. The general clinical impression that nifedipine is the agent most active in vascular tissue in relation to the myocardial effect is supported by data on the relative potencies of these three agents on blood perfused dog preparations and by a comparison of the potency on rat vascular (portal vein) versus myocardial effects. Nonetheless all three agents are highly active in the inhibition of K(+)-induced vascular contractions (nifedipine 10(-9) M to 10(-8) M; verapamil 10(-7) M to 10(-6) M; and diltiazem 5 x 10(-7) M to 10(-6) M; concentrations for 50% inhibition of K(+)-induced vascular contractions in rat or rabbit aorta; comparative data for resistance vessels not available). The clinical impression that verapamil and diltiazem are more active on nodal tissue is also supported by a comparison of potencies on blood perfused dog nodal preparations in comparison with effects on coronary flow, with verapamil and diltiazem being approximately 10x more potent on the AV node than increasing coronary blood flow, so that the nodal effect is first detected. These basic pharmacological properties explain why all these three agents have clinical effects relevant to inhibition of vascular contraction (antihypertensive and antianginal effects) and only verapamil and diltiazem have clinically relevant inhibitory effects on the AV node (inhibition of supraventricular tachycardias). The comparative potencies of verapamil, diltiazem, and nifedipine in angina and hypertension will be examined in Parts II and III of this review.
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PMID:Calcium channel antagonists, Part I: Fundamental properties: mechanisms, classification, sites of action. 285 70


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