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Query: UMLS:C0018801 (heart failure)
 72,216 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

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

Five patients developed coronary artery spasm during open heart surgery in our institute between 1984 and 1988. One patient was undergoing coronary artery bypass grafting and the other four valvular surgery or surgery for congenital heart disease. In one of the patients undergoing non-coronary surgery, the preoperative induction of right coronary artery spasm by ergonovine had been documented angiographically while the remaining three patients did not possess organic or functional coronary disease. All five patients exhibited a sudden onset of hemodynamic collapse with ventricular tachyarrhythmias or ST elevation during the early period of reperfusion, the time to onset being 89.2 +/- 84.8 minutes after unclamping of the aorta. In addition, contraction of the right ventricular free wall was severely impaired. Although one patient died due to left ventricular rupture caused by direct cardiac massage, the early mortality thus being 20 per cent, the other four were successfully treated with the intravenous administration of nitroglycerin and diltiazem. Three patients required the assistance of intraaortic balloon pumping for severe cardiac failure. Thus, during open heart surgery, coronary artery spasm can occur even in patients without organic coronary lesions and the possible mechanisms of this condition are discussed herein.
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PMID:A new aspect of coronary artery spasm induced by cardiac surgery. 196 Aug 98

An anaphylactic reaction in the isolated perfused heart is characterized by a drastic coronary constriction, arrhythmias, and an impairment of contractility. In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to ascertain the electrocardiographic and cardiovascular changes during systemic hypersensitivity reactions. In addition, an attempt was made to differentiate cardiac from respiratory events. In guinea pigs, sensitization was produced by s.c. administration of ovalbumin together with Freund's adjuvant solution. Fourteen days after sensitization, the effects of an i.v. infusion of ovalbumin were tested in the anesthetized guinea pigs, which were ventilated with room air or 100% oxygen. A second administration of the antigen induced the development of cardiovascular collapse, leading to death within 12 min. Within 3 min, cardiac output decreased by 90% and end-diastolic left ventricular pressure increased significantly, indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, arrhythmias occurred in the form of atrioventricular block. Left ventricular contractility declined continuously within the first 4 min. Finally, after 4 min, blood pressure steadily decreased. During ventilation with room air, severe hypoxia developed, with arterial PO2 decreasing from 94 mmHg to 14 mmHg after 3 min. However, under ventilation with 100% oxygen, a dissociation between cardiac damage and respiratory distress occurred. Myocardial ischemia and signs of cardiac failure preceded the development of hypoxia by a significant time interval. It is to be concluded that cardiac damage is a primary event in anaphylactic shock. Furthermore, the electrocardiographic signs of ischemia are interpreted as a result of coronary artery spasm.
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PMID:Systemic anaphylaxis--separation of cardiac reactions from respiratory and peripheral vascular events. 221 74

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

1. Verapamil remains the most widely used calcium antagonist for the treatment of cardiac arrhythmias. It is the most potent and effective drug for the acute treatment of paroxysmal supraventricular tachycardia particularly, circus movement tachycardia with or without pre-excitation. 2. As it is a powerful depressant of atrioventricular nodal conduction it reduces the ventricular rate in atrial flutter and fibrillation with reversion to sinus rhythm in a proportion of patients with these arrhythmias. Because verapamil does not increase airways resistance it can be used in patients with obstructive airways disease. The drug is also effective in supraventricular tachyarrhythmias following open-heart surgery and myocardial infarction. 3. It is not an effective drug against ventricular arrhythmias unless due to coronary artery spasm. The use of verapamil should be avoided in the presence of sick sinus node syndrome, clinical cardiac failure and treatment with other negative inotropic drugs.
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PMID:Verapamil in cardiac arrhythmias: an overview. 674 51

Severe ventricular dysfunction in a patient prevented weaning from cardiopulmonary bypass after myocardial revascularization. Calcium chloride and increasing doses of dopamine had no effect. Coronary vasospasm was diagnosed based on ST elevation and myocardial failure. Verapamil 0.5 mg, injected into the aortic root, was followed by a dramatic improvement in cardiac contractility and successful weaning from cardiopulmonary bypass without inotropic support.
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PMID:Failure to wean from cardiopulmonary bypass after myocardial revascularization: successful treatment with verapamil via the aortic root. 819 20

In the setting of chronic heart failure (CHF), therapy with angiotensin converting enzyme (ACE) inhibitors generally reduces serum aldosterone levels acutely. However, long-term ACE inhibition is associated with aldosterone suppression that is weak, variable, and unsustained, i.e. aldosterone 'escape'. Magnesium loss caused by aldosterone and by diuretics can contribute to coronary artery spasm and arrhythmias. Aldosterone can block noradrenaline uptake by the myocardium; extracellular catecholamines may lead to arrhythmias and ischaemia. Aldosterone has been shown to have an acute arrhythmogenic effect as well as a potential detrimental effect on baroreflex function, a marker of prognosis in CHF. Both angiotensin II and aldosterone may stimulate myocardial fibrosis, which is associated with a higher incidence of malignant ventricular arrhythmias. ACE inhibition initiated early in the progression of CHF may prevent development of patchy myocardial fibrosis and its inherent arrhythmias and thus reduce the incidence of sudden death. Spironolactone therapy added to the regimen of an ACE inhibitor and diuretic can induce natriuresis and magnesium retention, increase myocardial noradrenaline uptake, and reduce the incidence of arrhythmias.
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PMID:Aldosterone escape during ACE inhibitor therapy in chronic heart failure. 868 54

In chronic heart failure, angiotensin-converting enzyme inhibitors produce an acute decrease in aldosterone levels. Long-term angiotensin-converting enzyme inhibition is, however, associated with aldosterone suppression that is weak, variable, and unsustained (ie, aldosterone escapes). The possible harmful effects of this residual aldosterone are multiple Magnesium loss caused by aldosterone and by diuretics could contribute to coronary artery spasm and arrhythmias. Aldosterone blocks norepinephrine uptake by the myocardium; extracellular catecholamines may, therefore, lead to arrhythmias and ischemia. Aldosterone has been shown to have an acute arrhythmogenic effect as well as a detrimental effect on parasympathetic and baroreflex function. Both angiotensin II and aldosterone stimulate myocardial fibrosis, which may lead to a higher incidence of malignant ventricular arrhythmias. Spironolactone therapy added to the regimen of an angiotensin-converting enzyme inhibitor and diuretic has been shown to cause natriuresis, magnesium retention, increased myocardial norepinephrine uptake, and reduced incidence of ventricular arrhythmias. It may well be that residual aldosterone mediates many harmful effects in chronic heart failure and that to optimize the benefit of blocking the renin-angiotensin-aldosterone system may require specific blockade of residual aldosterone as well as traditional angiotensin-converting enzyme inhibition.
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PMID:Aldosterone escape during angiotensin-converting enzyme inhibitor therapy in chronic heart failure. 879 5

Neuropeptide Y (NPY) has been recently characterised as one of the strongest circulating vasoconstrictor peptides, its elevated level may cause coronary artery spasm and increase of peripheral vascular resistance. All this contributes to ischemic myocardial damage and decrease of regional and global left ventricular function. The aim of the study was the examination of NPY plasma levels in patients with acute myocardial infarction (AMI) after thrombolytic therapy with or without reperfusion. The survey was made in 82 patients with AMI after thrombolytic therapy: 40 of them without reperfusion and 42 with reperfusion. The control group consisted of 20 healthy persons. Plasma levels of NPY were measured before thrombolysis, then 1, 3 and 5 days after, using a radioimmunologic method. All patients were treated with aspirin, glyceryl trinitrate and thrombolytic therapy (TT) with alteplase (r-TPA). In patients with AMI, NPY plasma levels were normal before and 1 day after TT, and were significant elevated 3 days after TT 5 days after TT, plasma NPY levels were still high in patients without reperfusion, but they decreased in patients with reperfusion. There was significant negative correlation between NPY level and left ventricular ejection fraction measured 5 days after AMI. During 30-days follow up systolic dysfunction of left ventricle with ejection fraction under 40% occurred in 21 patients and in 11 of them clinical symptoms of heart failure were observed. Using the multivariable regression analysis we showed that NPY concentration over 60 pg/ml is the independent factor leading to left ventricle systolic dysfunction. The results of our study suggest the contribution of NPY to the left ventricular remodeling after AMI.
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PMID:[Plasma levels of neuropeptide Y i patients with current myocardial infarction]. 1150 45


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