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

Myocardial dysfunction after hypothermic protection has been linked to various mechanisms. Coronary vasospasm in particular may be responsible for ischemic injury during reperfusion. Herein we hypothesized that coronary arteries (CA) sustain a cold-induced contraction during hypothermia mediated by a protein tyrosine kinase (PTK)-/protein tyrosine phosphatase (PTP)-dependent pathway. Isolated newborn lamb CA rings were studied in a tissue bath for isometric contraction during 2-h profound (17 degrees C) or ultra-profound (7 degrees C) hypothermia. In parallel, protein tyrosine phosphorylation was evaluated by use of the Western blot technique. Na-orthovanadate (SOV) and genestein (GEN) were used separately and in combination to evaluate the effect of PTK/PTP activation on CA contraction and tyrosine phosphorylation during cooling (17 or 7 degrees C) vs 37 degrees C. Cooling from 37 to 7 degrees C induced transient contraction at approximately 17 degrees C (29% KCl response), which was more prominent during rewarming to 37 degrees C (36% KCl). Cooling to 17 degrees C resulted in sustained contraction (7-10% KCl), which was reversible upon rewarming. Cold-induced contraction was significantly enhanced by SOV (7- to 10-fold at 17 degrees C; 2-fold at 7 degrees C) and abolished by GEN. Concurrently, tyrosine phosphorylation of 33-, 45-, and 104-kDa proteins increased during cooling (35-100% at 17 degrees C; 46-66% at 7 degrees C). Tyrosine phosphorylation was similarly enhanced by SOV (1.7- to 2.3-fold at 17 degrees C; 2.9- to 3.9-fold at 7 degrees C) and abolished by GEN in the presence or absence of SOV. These results support a prominent role for the PTK/PTP signal transduction pathway in the coronary artery cold-induced contraction. This information provides one possible biomolecular mechanism linked to ischemia/reperfusion pathophysiology of CA in neonatal hearts exposed to hypothermic myocardial protection.
 ...
PMID:Phosphorylation in coronary artery cold-induced contraction in the newborn lamb. 1133 88

Paroxysmal atrial fibrillation is described in a patient that was consistent with the clinical history developed after induction of coronary artery spasm. The mechanism appeared to be sinus node artery spasm inducing sinus node ischemia. Coronary artery spasm can be a cause of paroxysmal atrial fibrillation.
 ...
PMID:Coronary artery spasm-induced paroxysmal atrial fibrillation--a case report. 1151 96

We evaluated coronary stenting in nine patients with clinically severe, angiographically documented spasm refractory to aggressive pharmacologic management. No patient subsequently developed unstable ischemia requiring hospitalization as a consequence of recurrent spasm within the stent. Mechanisms of therapeutic failure included both persistent spasm and spasm in a different artery in one patient. Restenosis occurred in three patients who subsequently underwent repeat revascularization. In the rare, carefully selected patient, stents may represent an adjunct in the management of focal coronary artery spasm, although currently medical therapy remains the standard initial approach.
 ...
PMID:Stenting for coronary artery spasm. 1197 27

A 68-year-old man with good left ventricular function underwent subtotal gastrectomy for gastric cancer under general anesthesia. Twenty minutes after the start of surgery, ST-segment depression was noted on the electrocardiogram monitor without change in the hemodynamic state. Intravenous isosorbide dinitrate relieved the electrocardiographic signs of ischemia. Short episodes of the ST-segment depression recurred 5 times despite intravenous isosorbide dinitrate and nicorandil. Echocardiography immediately after the surgery revealed hypokinesia of the anterior, septal and apical segments with an ejection fraction of 48%, suggesting acute myocardial infarction or the "Takotsubo"-shaped cardiomyopathy. However, a day after surgery, echocardiography showed improvement of regional wall motion with an ejection fraction of 57%. Coronary angiography showed normal coronary arteries on the 22nd day after the surgery. Patient manifested occlusive coronary artery spasm on ergonovine provocative test. We would like to stress that perioperative coronary artery spasm may demonstrate ST-segment depression and may result in severe consequences, regressive but relatively prolonged, in left ventricular function.
 ...
PMID:[A case of intraoperative repeated coronary artery spasm with ST-segment depression]. 1242 17

A case of chest pain in a 31-year-old woman after vaginal delivery with epidural analgesia during sulprostone administration is described. Chest pain occurred shortly after sulprostone was started and disappeared when sulprostone was stopped. Ischaemia related data were negative. Angiographically coronary arteries were normal. Coronary artery spasm aetiology was retained. Sulprostone pharmacology is summarized. Coronary artery effects are compared with literature reports. Recommendations before sulprostone use are underlined.
 ...
PMID:[Chest pain and sulprostone during postpartum hemorrhage]. 1247 87

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
 ...
PMID:Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder. 1524 Apr 8

Silent myocardial ischemia is recognized as a common manifestation after percutaneous coronary interventions possibly due to induction of coronary artery spasm. A 54-year-old man was performed primary percutaneous transluminal coronary angioplasty with the diagnosis of acute myocardial infarction. His 18-hour control electrocardiogram showed big-notched inverted T waves in precordial, III, and aVF leads without any chest pain. These bizarre electrocardiographic findings were restored after a brief period indicating silent ischemia that is caused by coronary artery spasm.
 ...
PMID:Transient silent ischemia after percutaneous transluminal coronary angioplasty manifested with a bizarre electrocardiogram. 1600 1

Mechanisms underlying coronary spasm are still poorly understood. The aim of the study was to assess the hypothesis that fluctuations in the development of coronary spasm might reflect inputs from the adjacent esophageal system. We enrolled patients admitted to the coronary care unit for episodes of nocturnal angina. Seven patients with variant angina and five with coronary artery disease (CAD) had concurrent ECG and esophageal manometric monitoring. ECG monitoring documented 28 episodes of ST elevation in variant angina patients and 16 episodes of ST depression in CAD patients. Manometric analysis showed that esophageal spasms resulted remarkably more frequently in variant angina patients (143 total spasms; individual range 9-31) than in CAD patients (20 total spasms; individual range 0-9; P < 0.01). Time series analysis was used to assess fluctuations in the occurrence of abnormal esophageal waves and its relationship with spontaneous episodes of ST shift. Episodes of esophageal spasm in CAD were sporadic (<1 in 30 min) and not related to ECG-recorded ischemia. In the variant angina group, esophageal spasms were time related to ischemia (>1 into 5 min before ECG-recorded ischemia) (P < 0.05). A bidirectional analysis of causal effects showed that the influence processes between esophageal and coronary spasms were mutual and reciprocal (transfer function model, P < 0.05) in variant angina. We concluded that in variant angina patients, episodes of esophageal spasms and myocardial ischemia influenced each other. Mechanisms that cause esophageal spasm can feed back to produce coronary spasm. Coronary spasm may feed forward to produce additional episodes of esophageal spasm.
 ...
PMID:Coronary spasm reflects inputs from adjacent esophageal system. 1638 92

It is believed that myocardial ischemia-reperfusion injury is related to increased free radical generated and intracellular calcium overload especially during the period of reperfusion. The pineal secretory product, melatonin, is known to be a potent free radical scavenger, antioxidant and can inhibit the intracellular calcium overload. In this review, we have summarized the fundamental of cardiac ischemia-reperfusion injury and the effects of melatonin on myocardial damage that related to cardiac ischemia-reperfusion injury. The total antioxidant capacity of human serum is related to melatonin levels. Incidence of sudden cardiac death is high in the morning hours. It has been shown that melatonin levels are significantly low at these times and patients with coronary heart disease have lower than normal individuals. These findings thought that melatonin would be valuable to test in clinical trials for prevention of possible ischemia-reperfusion-induced injury, especially life threatening arrhythmias and infarct size, effecting life quality, associated with thrombolysis, angioplasty, coronary artery spasm or coronary bypass surgery.
 ...
PMID:[Myocardial ischemia-reperfusion injury and melatonin]. 1694 25

We report two cases of transient coronary artery ischemia manifested as chest discomfort with ST-segment elevation in inferior leads during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation. This unexpected complication was resolved by intravenous administration of nitrates. All patients exhibited normal coronary arteries in angiography. A neurally mediated pathway activated by the mechanical effects of the transseptal puncture on the interatrial vagal network leading to coronary artery spasm may be considered as a possible explanation of this phenomenon. Coronary artery embolism following the transseptal procedure represents a different underlying mechanism.
 ...
PMID:ST-segment elevation induced during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation. 1704 45


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>