Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Ischemia is suspected to occur frequently in patients with HCM and may result from various mechanisms, for example decreased coronary flow reserve, disease of small intramuscular arteries, "inadequate' size of coronary arteries relative to hypertrophied myocardium, diminution of coronary flow during systole, compression of septal perforator arteries during systole, coronary artery spasm, and co-existent atherosclerotic CAD, which can be present in up to a quarter of HCM patients above 45 years of age. The diagnosis of CAD in patients with HCM is difficult to make on clinical grounds, secondary to the high frequency of angina in patients with HCM without CAD. Pharmacological stress echocardiography is promising but needs to be further studied; stress thallium imaging is beset with frequent false positive results. At this time, coronary angiography remains the only reliable test for the definitive diagnosis of co-existent CAD in HCM. Beta-blockers and verapamil may help in relieving symptoms and silent ischemia in patients with HCM; in those with coexistent CAD and resistant symptoms, CABG alone or in combination with left ventricular myectomy or mitral valve replacement has been recommended.
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PMID:Ischemia and atherosclerotic coronary artery disease in patients with hypertrophic cardiomyopathy: a review of incidence, pathophysiological mechanisms, clinical implications and management strategies. 882 2

Although rotational ablation has been successful in the treatment of complex coronary lesions, periprocedural complications of microvascular-mediated ischemia (slow flow or no reflow) and coronary vasospasm may occur. In an attempt to reduce such complications, a drug cocktail consisting of a combination of verapamil 10 micrograms/ml, nitroglycerin 4 micrograms/ml, and heparin 20 U/ml was infused in 21 consecutive patients with AHA/ACC Type B2 and C lesion morphology. A total of 27 lesions were treated, with a procedural success rate of 95%. One patient required emergency bypass surgery. Coronary vasospasm occurred in 7% (2/27 lesions). Only one lesion (3.7%) was associated with a transient reduction in TIMI flow that resolved within 5 min, and none had classical no-reflow. No patient developed intraluminal thrombus, and none had hypotension requiring inotropic support. All patients had prophylactic temporary pacemakers inserted. All RCA and circumflex lesions and 50% of LAD stenoses required transient pacing. A "cocktail" infusion of verapamil, nitroglycerin, and heparin mixed in pressurized saline delivered through the 4-French Teflon sheath of the Rotablator system during rotational ablation is associated with high success and low complication rates. Transient AV block is frequent, especially when treating RCA and circumflex arteries; therefore, prophylactic pacing is indicated.
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PMID:Cocktail attenuation of rotational ablation flow effects (CARAFE) study: pilot. 887 32

The existence of coronary endoarterial cushions (CEC) in the human heart as nonpathological, functional entities has been debated, and CEC have been sparsely reported in animals. Arterial cushions are localized thickenings that protrude into the lumen of specific arteries. We have identified CEC in the rhesus monkey, dog, sheep, goat, pig, rabbit and rat, and in the human heart. Two distinct types are described: the ovoid CEC arranged singly, in pairs, or in groups of three to four, and the less common polypoid CEC seen primarily in humans. The highest incidence of CEC in rabbits and humans was in the left ventricle in arteries 150-488 microns in diameter. Light and electron microscopy demonstrated intimal location with smooth muscle cells surrounded by ground substance, collagen and elastin fibers in a highly organized pattern. Nerve fibers identified by their immunoreactivity with antiserum to the vasodilatory calcitonin-gene-related peptide contacted the CEC along the tunica media and were occasionally seen within CEC. Arrangement and histological composition of CEC suggest a role in the regulation of local blood flow and myocardial perfusion. In human hearts, the CEC density index correlated highly with the degree of heart disease. In subjects with high heart disease rating, increased connective tissue, lipid-like infiltration and calcification was seen within CEC, and foam cells were present in CEC of obese rabbits. This suggests that CEC in coronary arteries could be predisposed sites of atherosclerosis, and that injured CEC can cause coronary artery spasm and ischemia. We conclude that CEC occur in animals and humans as innervated intimal smooth muscle cushions that might have a role in myocardial perfusion and heart disease.
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PMID:Intramyocardial arterial cushions of coronary vessels in animals and humans: morphology, occurrence and relation to heart disease. 892 19

A 70-year-old female was referred due to chest pain and cardiogenic shock. Echocardiogram showed ventricular septal perforation (VSP) with large left to right shunt. ECG indicated ischemia on the left anterior descending region. Instantaneous coronary angiogram was done under the support of IABP. Neither obstructive nor stenotic lesions were found in the coronary arteries. Coronary artery spasm was a likely cause of VSP. The patient underwent emergency surgery within 12 hours from the onset. The VSP, 2 cm in diameter, was located on the postero-apical portion of the ventricular septum. The defect was closed by endocardial patch method using an equine pericardium. Postoperative course was uneventful, and the patient was transferred 3 weeks after the operation.
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PMID:[Ventricular septal perforation due to coronary artery spasm--a case report]. 921 97

Intravenous dipyridamole is a potent coronary vasodilator that has been extensively investigated over the past several years in the noninvasive assessment of patients with suspected coronary artery disease when exercise cannot be performed or is suboptimal. As an alternative to exercise studies, dipyridamole has been used in combination with different cardiac imaging techniques such as echocardiography, thallium scintigraphy, and radionuclide ventriculography. Extensive experience has been obtained with dipyridamole thallium-201 imaging for coronary artery disease screening, risk stratification, and prognosis after an acute coronary event. However, experience with the use of dipyridamole in combination with two-dimensional echocardiography has been limited. Dipyridamole increases coronary blood flow in nondiseased coronary vessels relative to coronary vessels with significant luminal narrowings. These provide the basis for detecting regional differences in flow by using different cardiac imaging techniques. Two-dimensional echocardiography would show regional wall-motion abnormalities in response to those regional differences in coronary blood flow. In this article, the most commonly used protocols, safety, and practicability of dipyridamole echocardiography are reviewed. As an alternative to exercise, dipyridamole echocardiography shares all the indications of a standard exercise test. Clinical applications of dipyridamole echocardiography include coronary artery disease screening, suspected coronary artery spasm, postmyocardial infarction risk stratification, evaluation of percutaneous transluminal coronary angioplasty results, and prognosis following an acute coronary event. Compared to conventional (ECG) exercise testing, dipyridamole echocardiography appears to be equally sensitive but more specific. Compared to atrial pacing, dipyridamole provokes ischemia at a lower rate pressure product and results in a greater ST segment depression suggesting that dipyridamole induces more profound myocardial ischemia than atrial pacing. Dipyridamole thallium and exercise thallium have shown to be equally sensitive and specific in the assessment of coronary artery disease. High dose dipyridamole echocardiography appeared to be equally sensitive and more specific. Experimental studies have demonstrated that dobutamine appears to be a more powerful pharmacological agent in inducing wall-motion abnormalities. Dipyridamole echocardiography as compared to stress echocardiography offers the advantage of obtaining better quality postintervention images. With regard to sensitivity and for coronary artery disease diagnosis, both techniques appear to render similar results. Although further studies are needed, the available data indicates that cardiac ultrasound imaging prior to and following the intravenous administration of dipyridamole may be an attractive alternative to thallium perfusion imaging in the clinical setting, particularly when radionuclide capabilities are not present.
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PMID:Dipyridamole echocardiography. 1014 77

Myocardial hibernation is a state of persistently impaired left ventricular function in patients with coronary artery disease that was thought to be caused by a chronic reduction in resting myocardial blood flow in a segment subtended by a diseased coronary artery. However, recent studies using positron emission tomography have demonstrated that absolute myocardial blood flow (ml/min/g) to hibernating myocardium is within normal limits in most patients. If resting flow is not reduced, one must therefore suspect an alternative "trigger" for hibernation that is still a consequence of coronary artery disease and ischemia. We suspect that hibernating myocardium may be the result of repetitive myocardial stunning. Myocardial stunning is the reversible contractile dysfunction occurring after a period of myocardial ischemia that persists for a period of time despite the return of blood flow to normal. Myocardial stunning has been demonstrated in humans in the setting of thrombolysis, coronary angioplasty, coronary artery bypass surgery, and coronary artery spasm. Furthermore, stunning has been demonstrated after exercise in patients with coronary artery disease, and recent studies have provided evidence that repetitive episodes of exercise-induced ischemia can lead to cumulative and prolonged left ventricular dysfunction.
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PMID:Myocardial hibernation vs repetitive stunning in patients. 1034 65

Chest pain following successful percutaneous coronary interventions is a common problem. Although the development of chest pain after coronary interventions may be of benign character, it is disturbing to patients, relatives and hospital staff. Such pain may be indicative of acute coronary artery closure, coronary artery spasm or myocardial infarction, but may also simply reflect local coronary artery trauma. The distinction between these causes of chest pain is crucial in selecting optimal care. Management of these patients may involve repeat coronary angiography and additional intervention. Commonly, repeat coronary angiography following percutaneous transluminal coronary angioplasty (PTCA) in patients with chest pain demonstrates widely patent lesion sites suggesting that the pain was due to coronary artery spasm, coronary arterial wall stretching or was of non-cardiac origin. As reported by the National Heart, Lung and Blood Institute PTCA Registry, 4.6% of patients after angioplasty have coronary occlusions, 4.8% suffer a myocardial infarction, and 4.2% have coronary spasm. The frequency of chest pain after new device coronary interventions (atherectomy and stenting) seems to be even higher. However, only the minority of patients with post-procedural chest pain have indeed an ischemic event. Therefore, the vast majority of patients have recurrent chest pain without any signs of ischemia. There is some evidence that non-ischemic chest pain after coronary interventions is more common after stent implantation as compared to PTCA (41% vs. 12%). This may be due to the continuous stretching of the arterial wall by the stent as the elastic recoil occurring after PTCA is minimized. In conclusion, chest pain after coronary interventional procedures may potentially be hazardous when due to myocardial ischemia. However, especially after coronary stent placement, cardiologists must consider "stretch pain" due to the overdilation and stretching of the artery caused by the stent in the differential diagnosis. Clinically, it is, therefore, important to recognize that in addition to ischemia-related chest pain other types of chest pain do exist with cardiac origin.
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PMID:Chest pain after coronary interventional procedures. Incidence and pathophysiology. 1037 98

The conceptual model of the classical "ischemic cascade" has served cardiologists well for decades. It correctly predicts clinical findings during imaging stress testing in the presence of coronary artery disease or epicardial coronary artery spasm, where perfusion and wall motion abnormalities provide a substantially higher sensitivity than ECG changes. However, empirical experience has taught us that stress-induced ischemic-like ECG changes, often accompanied by perfusion abnormalities, are the rule rather than the exception in pathophysiological conditions during which the occurrence of ischemia usually cannot be proven, characterized by angiographically normal arteries and reduced flow reserve, such as syndrome X, arterial hypertension and hypertrophic cardiomyopathy. These stress-induced "echocardiographically silent" ST segment changes may be associated with impaired coronary flow reserve and systemic endothelial dysfunction. In hypertrophic cardiomyopathy stress-induced ischemic-like ST segment depression is linked to higher long-term incidence of adverse events. It is entirely likely that our monolithic view of ischemia mirrored in the classical ischemic cascade should be integrated by the awareness of the reverse or alternative "ischemic" cascade best describing microvascular disease, with ECG changes coming first, perfusion abnormalities second, and echocardiographic changes usually being absent. Not all forms of myocardial ischemia are the same, and milder, patchy degrees of myocardial ischemia--as those hypothesized, but not proven, in microvascular angina--remain silent in its mechanical functional manifestations and may well represent a physiological scotoma of stress echocardiography. "Anatomic lies" on the ECG may be overturned into "physiologic truths" when coronary flow reserve or systemic endothelial function is considered.
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PMID:The alternative "ischemic" cascade in coronary microvascular disease. 1060 88

The incidence of provoked coronary spasm with the standard single spasm provocation test has been relatively low in patients with rest angina. The present study examined the clinical usefulness of a newly designed spasm provocation test, an intracoronary injection of acetylcholine (ACh) following an ergonovine (ER) test, in patients with rest angina who demonstrated low disease activity and atypical chest pain. Triple sequential spasm provocation tests were performed in 24 patients with atypical chest pain who had no ischemia and in 40 patients with rest angina who had distinct ischemia. Initially, an ACh test (20-100 microg) and then an ER test (40-64 microg) were performed and then, if no spasm was provoked, an intracoronary injection of ACh was given after the ER test to evaluate coronary spasm. Coronary spasm was defined as total or subtotal occlusion. In the 24 patients with atypical chest pain, no spasm was provoked by intracoronary injection of either ACh or ER, but coronary spasms were induced in 2 patients using the new method, with the remaining 22 not experiencing spasm (specificity of new method, 92%). In the 40 patients with rest angina, intracoronary injection of ACh induced coronary spasm in 22 patients (group I) and 6 (group II) demonstrated spasm with intracoronary injection of ER. Coronary spasm was not induced by either the ACh test or the ER test in 12 patients (group III). The intracoronary administration of ACh after the ER test provoked spasm in 11 of 12 patients. Diffuse spasms were provoked in 10 of 11 patients. In patients with rest angina, the frequency of chest pain attacks in 1 month experienced by patients in group III (0.8+/-0.8) was significantly lower than that of patients in group I (7.0+/-5.3, p<0.01) or II (3.5+/-2.3, p<0.05). No serious or irreversible complications related to this new combined method were observed. In conclusion, this method was safe and reliable for the induction of coronary spasm in patients with rest angina who may have low disease activity.
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PMID:New combined spasm provocation test in patients with rest angina: intracoronary injection of acetylcholine after intracoronary administration of ergonovine. 1095 50


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