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

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.
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PMID:Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta. 14 28

Calcium entry blockers are now widely employed in the treatment of cardiovascular diseases and perioperative hypertension. In patients with coronary heart disease nifedipine therapy should be continued perioperatively to avoid coronary artery spasm. Animal experiments have demonstrated that calcium entry blockers potentiate the neuromuscular blockade induced by nondepolarizing blocking agents. In patients, an atracurium-induced neuromuscular depression is prolonged by intravenous nifedipine. In this prospective clinical study we evaluated the effect of chronic oral nifedipine therapy on the duration of neuromuscular block by atracurium. Sixty patients anaesthetized with isoflurane in nitrous oxide/oxygen were recruited for this study. Thirty of these were on chronic oral nifedipine therapy and received their normal morning dose before premedication. The control consisted of 30 patients of similar age and status but not taking any calcium entry blockers. Monitoring included noninvasive blood pressure, heart rate, pharyngeal temperature, physical breathing parameters and neuromuscular transmission with a Datex Relaxograph TM ("train of four"-principle). After inducing hypnosis 0.5 mg/kg atracurium were administered for muscular relaxation. The duration of block from administration of the relaxant to recovery of first twitch height (T1) to 25% of control twitch height was registered as duration of initial block. When T1 reached 25% a repetition dose of 0.2 mg/kg atracurium was injected. The time till recovery of T1 to 25% was recorded as the duration of the repetition dose. Results were compared using Student's t-test for unpaired data. There was a significant prolongation of the duration of initial block from 38 min +/- 10 min in the control group to 46 min +/- 8 min in the therapy group (P < 0.01). The duration of the repetition dose rose from 30 min +/- 8 min in the control group to 38 min +/- 7 min in the therapy group (P < 0.001). Daily nifedipine doses varied from 10 mg in the morning to 40 mg divided into single doses with no influence on the prolongation of neuromuscular block. Our results confirm previous assumptions of synergistic effects of nifedipine and neuromuscular blocking drugs in patients. Chronic oral nifedipine therapy potentiates neuromuscular blockade by atracurium as does nifedipine intravenously. This effect should be considered in the treatment of cardiovascular diseases with nifedipine in the perioperative period.
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PMID:[Nifedipine prolongs a neuromuscular blockade caused by atracurium]. 144 9

A rapidly growing body of data supports the concept of in situ regulation of vascular tone: the ability of vasoactive substances to regulate vascular tone at their site of production within the wall of the vasculature. Sufficient data exist to suggest that ineffective production or response to endothelium-dependent vasodilator substances, or excessive production or responsiveness to endothelium-dependent vasoconstrictor substances may play an important role in cardiovascular disorders such as hypertension, coronary artery spasm, restenosis following coronary angioplasty, and congestive heart failure. The present review summarizes data which support the concept that endothelin, a potent vasoconstrictor produced by the endothelium, may play a role in the excessive vasoconstriction of heart failure. Increased circulating plasma endothelin may be particularly relevant to the range of pulmonary vasoconstriction encountered in congestive heart failure, with a correlation revealing that the greatest increase of plasma endothelin occurs in patients with marked pulmonary hypertension within the congestive heart failure patients studied.
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PMID:The potential role of endothelin as a vasoconstrictor substance in congestive heart failure. 146 46

A case of a 57-year-old man with hypertension and stable angina, on aspirin therapy, who was treated for epistaxis with intranasal cocaine, and who subsequently suffered a non-Q wave myocardial infarction is reported. Of note, the cocaine was administered in a manner which differs from that advocated in standard references. Specifically, intranasal packing soaked with 4% cocaine was left in place with continuous nasal mucous membrane contact over 5 to 6 hours. The authors speculate that myocardial infarction occurred on the basis of coronary artery spasm. This case should alert practitioners to myocardial ischemia occurring as a complication of the therapeutic use of intranasal cocaine for the treatment of epistaxis.
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PMID:Myocardial infarction associated with inappropriate use of topical cocaine as treatment for epistaxis. 158 32

Coronary artery spasm plays an important role in acute ischemic events, and it has a close relationship with coronary atherosclerosis. Thus we attempted to determine the most significant risk factor for coronary artery spasm. Among 3000 consecutive patients who underwent coronary cineangiography with ergonovine maleate testing, 330 with typical angina pectoris (group 1) and 294 with old myocardial infarction (group 2) were studied. We divided each group into three or four subgroups according to the presence of fixed organic stenosis (FOS+) or a positive reaction to ergonovine maleate (coronary artery spasm [CAS]+). We examined the relationship between coronary artery spasm and eight coronary risk factors: age, sex, hypertension, diabetes mellitus, smoking, and serum cholesterol, uric acid, and high-density lipoprotein cholesterol levels. The proportion of smokers in the subgroups with CAS(+) was significantly higher than in the subgroups with CAS(-)(p less than 0.01). There was no correlation between smoking and fixed organic stenosis. According to the results of multiple regression analysis, there was a positive correlation between smoking and CAS(+) and between serum high-density lipoprotein cholesterol levels and CAS(+)(p less than 0.01). Thus we concluded that smoking is the most significant risk factor in discriminating between patients with and without coronary artery spasm.
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PMID:Statistical analysis of clinical risk factors for coronary artery spasm: identification of the most important determinant. 161 25

Local and systemic effects of intracoronary (two bolus injections of 25 micrograms at 3-min intervals) ergonovine were determined in 60 patients with angiographic non-spastic normal coronary arteries and were compared with the most usual intravenous ergonovine dose to induce coronary artery spasm (incremental doses of 50, 100 and 200 micrograms at 3-min intervals). The mean diameter of the vessels was reduced by 15% after selective injections (baseline 2.38 +/- 0.7; after intracoronary ergonovine 2.02 +/- 0.6 mm; p less than 0.001) and no significant changes were induced in the heart rate (before 80 +/- 15; after 79 +/- 15 beats/min) and systolic aortic pressure (before 147 +/- 27; after 149 +/- 28 mmHg). Following intravenous administration, the mean coronary diameter decreased by 20% (1.90 +/- 0.6 mm; p less than 0.01 vs intracoronary dose) and the heart rate diminished slightly (76 +/- 12 beats/min; p less than 0.01). Nevertheless, the systolic aortic pressure did increase by 16% (171 +/- 28 mmHg; p less than 0.001). No major complications were observed and the appearance of side effects was minimal. Thus, the intracoronary delivery route, at the applied dosage, induces lesser vasoconstriction than usual intravenous administration, and systemic effects, such as hypertension, are avoided.
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PMID:[The local and systemic effects of intracoronary ergonovine in patients with normal and nonspastic coronary arteries. A comparison with the intravenous ergonovine test]. 192 54

A case of a postpartum myocardial infarction in a 27-year-old black multiparous woman is presented. The patient had postpartum pregnancy-induced hypertension in a previous pregnancy. Her most recent pregnancy and immediate postpartum period had been uncomplicated, and she had been sent home with bromocriptine to suppress lactation. Ten days postpartum, she presented with severe hypertension followed by cardiac arrest. Subsequent coronary catheterization revealed no evidence of coronary atherosclerosis but showed a 60-70% stenotic plaque in the left anterior descending artery, possibly secondary to coronary artery spasm. A review of all previously reported cases of postpartum myocardial infarction is presented in an effort to identify the possible etiology of this event and to consider the role of bromocriptine. The most common associated finding in all cases was a history of pregnancy-induced hypertension, which may have been associated with a predisposition to coronary vasospasm. The compounding role of ergot derivatives on vasospasm is considered.
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PMID:Postpartum myocardial infarction in a patient receiving bromocriptine. 266 21

To assess the local and systemic intracoronary (IC) ergonovine maleate (EM), single or repeated 25 micrograms bolus injections were administered to 108 consecutive patients with chest pain and normal coronary arteriograms. Coronary artery spasm (CAS) was induced in 17 (15.7%) patients. None of these patients developed ST-segment depression, and ST-segment elevation appeared in only 6 (35.3%). In 59 of the 91 patients without CAS, both the IC and the intravenous (IV) EM arteriographic and hemodynamic effects were compared. The mean diameter of the vessels was reduced by 15% (p less than 0.001) after two single 25 micrograms ICEM injections. Only insignificant changes were induced in the heart rate (baseline 80 +/- 15; after ICEM 79 +/- 15 beats/min; p = NS) and systolic aortic pressure (baseline 147 +/- 27; after ICEM 149 +/- 28 mmHG; p = NS). Following 350 micrograms of cumulative IVEM, the mean coronary diameter decreased by 20% (p less than 0.01 vs. ICEM dose) and the heart rate diminished slightly (76 +/- 12 beats/min, p less than 0.01). However, the systolic aortic pressures did increase by 16% (171 +/- 28 mmHg; p less than 0.001). No major complications were observed. Thus, to induce CAS the IC delivery route appears to be safe, allows for more accurate titration, and adverse systemic effects, such as hypertension, are avoided.
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PMID:Effects of intracoronary injection of ergonovine on angiographic normal coronary arteries: study of 108 consecutive patients. 280 61

At present nitrates remain the initial treatment for relief or prevention of angina in patients with coronary artery disease. In cases where nitrates and beta blockers have been used and are ineffective for managing effort angina, calcium antagonists may be substituted or added to the beta-blocking treatment. When the predominant symptom is rest angina, and there is evidence suggesting coronary artery spasm, nitrates and a calcium antagonist can be effective therapy. In patients with heart block, bradyarrhythmias, heart failure, or hypertension nifedipine may be the drug of choice. In contrast verapamil merits choice when supraventricular tachycardia is present. Diltiazem appears intermediate between nifedipine and verapamil and may be particularly useful when hypotension or other side effects must be avoided.
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PMID:Calcium antagonists. 286 40

Intracoronary injection of acetylcholine has been shown to induce coronary spasm in patients with variant angina. To examine its sensitivity and specificity, incremental doses of acetylcholine (20, 50 and 100 micrograms into the left coronary artery and 20 and 50 micrograms into the right coronary artery) were injected into the coronary artery or arteries in 70 patients with variant angina (Group 1) (mean age 57 years) and 93 patients without variant angina or angina at rest (Group 2) (mean age 54 years). Forty patients of the latter group had atypical chest pain, 16 cardiomyopathy, 14 arrhythmia, 11 valvular disease, 7 stable effort angina due to advanced coronary artery disease, 3 congenital heart disease and 2 hypertension. A temporary cardiac pacemaker set at 40 to 50 beats/min was positioned in the right ventricle. Coronary spasm was defined as total occlusion or severe vasoconstriction associated with chest pain or ischemic ST changes on the electrocardiogram or both. In Group 1, acetylcholine induced spasm in 63 (90%) of the 70 patients in the artery or arteries predicted to be responsible for spontaneous attacks. In Group 2, acetylcholine induced coronary spasm only in one patient with effort angina and advanced coronary artery disease although lesser degrees of vasoconstriction (less than or equal to 75% of the luminal diameter) occurred in most patients after acetylcholine (specificity of acetylcholine thus was 99%). In conclusion, intracoronary injection of acetylcholine is sensitive and reliable for the induction of coronary spasm.
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PMID:Sensitivity and specificity of intracoronary injection of acetylcholine for the induction of coronary artery spasm. 304 96


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