PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Coronary Vasospasm”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1992

Two cases of variant form angina pectoris associated with myocardial bridge--a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge.

Myocardial bridge (MB) is a congenital anomaly of the coronary artery and may occur in 5 to 12% of the human population. However, the mechanism of MB-induced myocardial ischemia is still speculative. We report 2 cases of variant form angina pectoris associated with MB in which myocardial ischemia seemed to be related to the interaction between coronary perfusion and MB. In case 1, electrocardiography during anginal attack at rest showed ST elevation in the inferior leads and MB was observed after percutaneous transluminal coronary angioplasty at the site of the right coronary artery lesion following successful dilatation. In case 2, MB of the left anterior descending coronary was located in the identical portion where coronary vasospasm was induced by intracoronary acetylcholine injection, although ischemia during the spontaneous anginal attack was limited to the inferior area of myocardium. These 2 cases suggest that MB can be, at least in some patients, one of the possible causes of the endothelial damage which seems to be related to coronary vasospasm; this was documented in both cases.

Angina Pectoris, Variant↗
PubMed1977

Coronary vasospasm in angina pectoris.

Coronary angiography was performed during 34 angina attacks in thirty patients admitted because of recurrent angina at rest. Nineteen (seventeen with S-T segment elevation and two S-T depression) had angiograms during a spontaneous attack, eleven (nine with S-T elevation and two with S-T depression) during an attack induced by intravenous ergonovine maleate. Control coronary angiograms showed a wide range of atherosclerotic obstruction, from normal vessels to severe triple-vessel disease. During the anginal attack, all patients with S-T segment elevation had vasospasm localised to one of the major branches, often resulting in complete occlusion. Attacks with S-T segment depression were seen only in patients with double or triple vessel disease, and here the vasospasm generally affected coronary branches without causing complete occlusion. When appropriately searched for, vasospastic angina seems to be common.

Adult↗
PubMed1992

Can free radicals induce coronary vasospasm and acute myocardial infarction?

Spontaneous acute occlusion of the coronary artery produces regional myocardial ischemia and infarction. This coronary occlusion could be due to rapid progression of atherosclerosis or vasospasm. The factors that can precipitate an acute attack of myocardial infarction or coronary spasm are not known. It is proposed that a stress-induced rise of unesterified arachidonic acid could trigger a leukocyte respiratory burst with the release of free radicals such as superoxide anion (O2-), hydrogen peroxide, hydroxyl radical, and singlet oxygen. These free radicals have the ability to inhibit prostacyclin (PGI2) formation and enhance the breakdown of endothelium-derived vascular relaxing factor (EDRF) which are potent vasodilators and platelet anti-aggregators. This may lead to rapid progression of atherosclerosis or coronary vasospasm leading to acute myocardial infarction. If this is true, free radical quenchers and inhibitors of leukocyte oxidative burst may be useful in the prevention of progression of atherosclerosis and coronary vasospasm.

Animals↗
PubMedDate not supplied

The effects of distension of the small intestine on myocardial blood flow in anaesthetised cats: possible relevance to coronary vasospasm.

The haemodynamic effects of distending the small intestine (with a balloon in the lumen) were examined in cats anaesthetised with chloralose. Particular attention was paid to blood flow changes in localised areas of the left ventricular wall (as assessed using the heated thermocouple technique). Intestinal distension led to an increase in systemic blood pressure but usually to a reduction in myocardial blood flow; no cardiac dysrhythmias were observed. When the effect of increased systemic (perfusion) pressure on blood flow was eliminated (using partial correlation coefficients) flow then bore a negative relationship to intestinal pressure, probably indicating constriction of the myocardial blood vessles. This may indicate that distension of hollow organs can lead to a visceral-cardiac reflex. The resulting coronary vasospasm might be one cause of pain in certain patients with angina pectoris.

Animals↗
PubMed1978

Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina.

To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.

Adult↗
PubMed1992

Preserved endothelium-dependent vasodilation at the vasospastic site in patients with variant angina.

Endothelial dysfunction has been implicated as a cause of coronary vasospasm in patients with variant angina. This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. It has been shown that SP evokes endothelium-dependent vasodilation with no direct effect on vascular smooth muscle in excised human coronary arteries. SP and ACH were infused into the coronary arteries in nine patients with variant angina in whom coronary arteriograms showed normal or mild atherosclerotic lesions. The vasomotor responses of coronary arteries were assessed by quantitative arteriography. ACH at a high dose (100 micrograms/min) provoked coronary vasospasm associated with anginal attack in all patients. In contrast, SP at graded doses (13.5, 40, and 135 ng/min) caused the dose-dependent and comparable increases in the coronary diameter at the spastic and control sites. ACH at a low dose (10 micrograms/min) also caused comparable vasodilation at the spastic and control sites in patients with normal coronary arteries. Coronary vasodilating responses to SP were comparable in patients with variant angina and those with atypical chest pain. The results indicate that endothelium-dependent vasodilation evoked with SP and ACH at the low dose was present at the vasospastic site in patients with variant angina. These findings suggest that the ACH-induced coronary vasospasm in patients with variant angina results from hyperreactivity of vascular smooth muscle to ACH but not from endothelial dysfunction.

Acetylcholine↗
PubMed1979

Coronary artery vasospasm: the likely immediated cause of acute myocardial infarction.

Features of infarction can be divided into two types--the spasmodic and the mechanical. The former (pre-infarct angina and emotional factors in infarction) seem readily explainable by spasm, and are similar to the findings in angina which prompted Heberden to consider angina as spasmodic. The mechanical features of infarction (association with thrombosis and arteriosclerosis, and severe and unremitting chest pain) seem to be the antithesis of spasm and probably account for the reluctance to consider spasm seriously in infarction. The injury-vasospasm hypothesis of acute myocardial infarction explains both spasmodic and mechanical features. Spasm represents a dominance of vasoconstricting over vasodilating forces. Coronary sclerosis can result in both ischaemia (vasodilating) and ischaemic injury-spasm (vasoconstricting). The fight-flight component of the autonomic nervous system is considered to be vasodilating, and the conservation-withdrawal portion to be vasoconstricting. Once spasm occurs, a new balance of forces obtains which can lead either to vasodilatation and relief of symptoms or to infarction.

Acute Disease↗
PubMed1992

Cocaine abuse: an expanding healthcare problem for the 1990s.

Cocaine, the most addictive recreational drug available, has increased in popularity and widespread use in the past decade. Crack, a new form of cocaine that is smoked, is purer and more rapidly absorbed into the vascular system, greatly increasing the risk of overdose. Cocaine produces many physiologic effects on the body systems. This case report focuses on two cardiovascular responses related to cocaine use: cardiomyopathy and coronary vasospasm. Cocaine abusers may present with complaints of chest pain or other nonspecific symptoms that require diligent assessment skills to be recognized as cocaine-related. Therefore, it is essential that nurses be knowledgeable about the effects of cocaine and the symptoms of cocaine abuse.

Adult↗
PubMed1992

Extraordinary unremitting endurance exercise and permanent injury to normal heart.

This hypothesis is that permanent cardiac injury could develop in some endurance athletes despite the absence of coronary atherosclerosis and ventricular hypertrophy. The proposed mechanism by which this injury could arise involves two physiological "vicious cycles". The first vicious cycle would occur between severe ischaemia and high catecholamines, the second would be between coronary vasospasm (induced by high catecholamines) and endothelial injury. The likelihood of the injury becoming permanent might increase if there is insufficient time between bouts of endurance exercise for regression of ischaemia and endothelial repair. Furthermore, magnesium ion deficiency, which can be induced by exercise, could exacerbate these vicious cycles and also contribute to catecholamine-induced thrombogenesis. In addition to ischaemia, there are several mechanisms, including the effect of free fatty acids liberated by the lipolytic effect of high catecholamines, that could cause direct myocardial injury.

Catecholamines↗
PubMed1975

Variant angina and sleep: a case report with therapeutic considerations.

A 33 year old male with three years of increasingly frequent nocturnal angina pectoris was found on ECG tape monitoring to develop marked ST segment elevation followed by coarse ventricular tachycardia with subsequent spontaneous termination of the arrhythmia. Further evaluation included normal maximal exercise tolerance test, normal coronary arteriography and left ventricular angiography. Continuous nocturnal EEG, ECG, and blood pressure recordings on nitrate therapy revealed normal sleep patterns, development of sinus tachycardia with minimal muscular movement and a normal circadian decline in blood pressure. Therapy with progressive doses of 2% Nitroglycerin ointment has prevented further breakthrough in nocturnal angina pectoris. The association of nocturnal angina and sleep stages and the possibility of altering the coronary vasospasm by approaching the central neurophysiologic trigger rather than the peripheral coronary arteries is discussed.

Adult↗
PubMed1992

Acute hemodynamic effects of carvedilol in comparison with propranolol in patients with coronary heart disease.

In a randomized, double-blind study oral doses of 50 mg carvedilol (Dilatrend) were compared with 40 mg propranolol in 16 male patients with coronary heart disease, CHD [12 without significant stenoses following percutaneous transluminal coronary angioplasty (PTCA), 4 with multivessel disease]. Bicycle ergometry in the supine position was performed before and 80 min after drug application; measurements were done at rest, during and after exercise. Clinically, the total exercise time and the onset of angina and exhaustion were noted, while the investigated hemodynamic parameters were heart rate, systemic and pulmonary pressures and resistances, cardiac index, and lower limb blood flow. Clinically, carvedilol improved the exercise tolerance more than propranolol as regards angina and exhaustion. Hemodynamically, carvedilol did not lead, as the classic betablocker propranolol does, to an increase in systemic or pulmonary resistance, to a decrease in cardiac output, or to an increase of the pulmonary capillary wedge pressure during exercise, but instead caused opposite changes. In contrast to propranolol, the post exercise lower limb blood flow had increased significantly. The differences in action between the two betablockers can be explained by the vasodilating properties of carvedilol. Due to these acute effects, carvedilol may be preferred to propranolol in the treatment of CHD patients with hypertension, peripheral occlusive artery disease, and/or coronary vasospasm.

Adrenergic beta-Antagonists↗
PubMed1992

Effect of K+ channel-modulating drugs on the vasoconstrictor responses of leukotrienes C4, D4 and angiotensin II in the guinea-pig isolated perfused heart.

1. The vascular actions of leukotrienes C4 (LTC4) and LTD4 in the guinea-pig isolated perfused heart were studied in the presence of potassium (K+) channel modulatory compounds. 2. Cromakalim (0.35-10 microM), a K+ channel activator, inhibited the vasoconstrictor responses of LTC4 (30 pmol), LTD4 (30 pmol) and angiotensin II (AII) (100 pmol) in a concentration-dependent manner. 3. Glyceryl trinitrate (10 mgl-1) and vasoactive intestinal peptide (10 nM) induced a similar vasodilator action to cromakalim in the isolated heart but had no effect on responses to LTC4 and LTD4. 4. The inhibitory action by cromakalim (10 microM) on the LTC4 (30 pmol) response could be reversed in the presence of an equimolar concentration of glibenclamide. However, glibenclamide (10 microM) only partially restored the LTD4 (30 pmol) actions. 5. Galanin (10 nM) and charybdotoxin (60 nM) had no effect on the vascular responses to LTC4 and LTD4 (30 pmol). 6. Inhibition by cromakalim of coronary vasospasm induced by vascular LTC4, LTD4 and AII appears to be separate from its vasodilator action and it is postulated that a cromakalim-sensitive mechanism in the coronary vasculature is important in the vasoconstrictor responses to LTC4, LTD4 and AII.

Angiotensin II↗