Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In protracted myocardial ischemia, sympathetic nerve endings undergo ATP depletion, hypoxia and pH(i) reduction. Consequently, norepinephrine (NE) accumulates in the axoplasm, because it is no longer stored in synaptic vesicles, and intraneuronal Na(+) concentration increases, as the Na(+)/H(+) exchanger (NHE) is activated. This forces the reversal of the Na(+)- and Cl(-)-dependent NE transporter, triggering a massive carrier-mediated release of NE and thus, arrhythmias. Indeed, NE overflow in myocardial ischemia directly correlates with the severity of arrhythmias. Histamine H(3)-receptors (H(3)R) have been identified as inhibitory heteroreceptors in adrenergic nerve endings of the heart. In addition to inhibiting NE exocytosis from sympathetic nerve endings, selective H(3)R agonists attenuate carrier-mediated release of NE in both animal and human models of protracted myocardial ischemia. Whereas H(3)R-mediated attenuation of exocytotic NE release involves an inhibition of N-type Ca(2+)-channels, H(3)R-mediated reduction of carrier-mediated NE release is associated with diminished NHE activity. In addition to inhibiting NE release, H(3)R stimulation significantly attenuates the incidence and duration of ventricular fibrillation. Although other presynaptic receptors also modulate NE release from sympathetic nerve endings, H(3)R stimulation reduces both exocytotic and carrier-mediated NE release, whereas alpha(2)-adrenoceptor agonists attenuate NE exocytosis but enhance carrier-mediated NE release. Furthermore, unlike adenosine A(1)-receptors, whose activation reduces both exocytotic and carrier-mediated NE release, H(3)R stimulation is devoid of negative chronotropic and dromotropic effects (i.e., sinoatrial and atrioventricular nodal functions are unaffected). Because excess NE release can trigger severe arrhythmias and sudden cardiac death, negative modulation of NE release by H(3)R agonists may offer a novel therapeutic approach to myocardial ischemia.
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PMID:Histamine H(3)-receptors: a new frontier in myocardial ischemia. 1068 93

The results of the NASPE Prospective Voluntary Registry are reported. A total of 3,357 patients were entered. For those undergoing atrioventricular (AV) junctional ablation (646 patients), the success rate was 97.4% and significant complications occurred in 5 patients. A total of 1,197 patients underwent AV nodal modification for AV nodal reentrant tachycardia, which was successful in 96.1% and the only significant complication was development of AV block (1%). Accessory pathway ablation was performed in 654 patients and was successful in 94%. Major complications included cardiac tamponade (7 patients), acute myocardial infarction (1 patient), femoral artery pseudoaneurysm (1 patient), AV block (1 patient), pneumothorax (1 patient), and pericarditis (2 patients). A total of 447 patients underwent atrial flutter ablation and acute success was achieved in 86% of patients. Significant complications included inadvertent AV block (3 patients), significant tricuspid regurgitation (1 patient), cardiac tamponade (1 patient), and pneumothorax (1 patient). Atrial tachycardia was attempted for 216 patients and the success rate was higher for those with right atrial (80%) or left atrial (72%) compared to those with septal foci (52%). A total of 201 patients underwent ablation for ventricular tachycardia. The success rate was higher for those with idiopathic ventricular tachycardia compared to those with ventricular tachycardia due to ischemic heart disease or cardiomyopathy. While the number of AV junction ablation were higher for those > 60 years of age, there was no significant difference in the success rate or incidence of complication comparing patients > or = 60 to those < 60 years of age. In addition, we found no differences in incidence of success or complications comparing large volume centers (> 100 ablation/year) with lower volume centers or between teaching and non-teaching hospitals.
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PMID:The 1998 NASPE prospective catheter ablation registry. 1087 89

Acute inferior wall infarction is frequently complicated by conduction disturbance, but the relationship between ischemia and atrioventricular (AV) conduction disturbance is not well understood. The present experiments were made on cats with heart efferent completely denervated. A, H and V waves were picked up by a template-machine algorithm from His bundle electrogram, AA interval (cardiac cycle length), AH interval (AV conduction time), HV and AV intervals were measured. Of 20 cats, 14 showed prolongation of AH interval (Group A), while not in 6 cats (Group B) after ligation of right coronary artery. A fast pacing of right atrium (AA interval = 267 ms) was produced in Group B and AH interval was also prolonged after ligation of the artery. By multiple-step pacing, the curve of AV nodal function shifted to the right, AH interval which induced AV nodal block was prolonged after ischemia. After reperfusion, AH interval was shortened both in Group A and B. The above results show that myocardial ischemia may cause abnormality of AV conduction and accommodation function. The abnormality appears to be a potential danger which will induce AV conduction block during tachycardia.
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PMID:[Atrioventricular conduction changes in acute ischemic and reperfused coronary artery of cats]. 1149 88

Drugs classified as calcium channel blockers (CHBs) are now among the most frequently prescribed drugs for the treatment of cardiovascular disease. Although the currently available CCBs have major differences in their structural and cardiovascular effects, they share the common property of blocking the transmembrane flow calcium ions through voltage gated L-type channels. These drugs have been approved for the treatment of hypertensive heart disease: they reduce left ventricular hypertrophy and improve its sequelae, such as ventricular dysrhythmias, impaired filling and contractility, and myocardial ischemia. Long-acting CCBs have been shown to reduce mortality and morbidity in elderly patients with systolic hypertension, appear to be extremely useful in patients with cyclosporin-induced hypertension, and can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus, renal disease, Raynaud's phenomenon or migraine. Long-acting dihydropyridine have been shown to be effective and safe in the treatment classic angina pectoris and vasospastic angina, supraventricular arrhythmias, particularly reentrant AV-nodal tachycardia, others to be beneficial in patients with congestive heart failure, and all of them have potential for decreasing atherogenesis.
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PMID:[Calcium channel blockers in the treatment of cardiovascular disease]. 1157 40

In the newly published WHO classification for tumors of the hematopoietic and lymphoid tissues, Hodgkin's disease has been renamed Hodgkin lymphoma, which reflects the recent confirmation of its germinal center B-cell origin. In the classification, nodular lymphocyte-predominant Hodgkin lymphoma has been added as a new entity with an excellent prognosis. For management of the disease, a risk-adapted classification is employed without staging laparotomy. In limited stages without risk factors, subtotal nodal irradiation with sophisticated techniques can cure more than 80% of patients. Multimodality therapy with chemo- plus radiotherapy can improve disease-free survival, but overall survival remains unchanged. In the intermediate stages with risk factors, chemo- plus radiotherapy is standard, with 3-4 cycles of ABVD and involved field irradiation. In advanced stages, chemotherapy plays a decisive role, with radiation therapy used as an adjuvant for bulky and/or slowly responding tumors. Long-term follow-up of cured Hodgkin patients has revealed increased incidences of solid malignancies and ischemic heart disease more than 15 years after therapy. Breast cancer and ischemic heart disease appear to be related to mantle irradiation, although sophisticated modern radiation therapy techniques are demonstrated to lower the incidence of these long-term morbidities. Meticulous radiation therapy remains the most effective tool for local control of Hodgkin lymphoma.
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PMID:[Hodgkin lymphoma]. 1204 26

Lewy bodies (LB) are characteristic pathological findings for idiopathic Parkinson disease, and extracranial organs have also been known to exhibit these structures. Clinically, the possible involvement of LB in cardiac dysfunction has attracted attention based on the findings of studies using [123I] metaiodobenzyl guanidine (MIBG) scintigraphy. The purpose of the present study was to investigate the possible involvement of LB in heart disease. A total of 40 autopsy cases consisting of Lewy body disease and Parkinson syndrome were examined. The former were cases with intracranial LB regardless of clinical symptoms, and the latter were cases with parkinsonism but without intracranial LB. The presence of heart disease or an atrial arrhythmia and the results of an MIBG scintigraphy study were clinically examined. The sinoatrial node was examined microscopically and immunohistochemically. The results showed that heart disease and atrial arrhythmia complications were more frequent in cases with Lewy body disease than in cases with Parkinson syndrome and that LB were frequently found in extracranial organs, especially in the sinoatrial nodal ganglion, in cases with Lewy body disease. In the current report, we hypothesized that neuronal changes involving LB in the sinoatrial nodal ganglion may cause arrhythmia and ischemic heart disease as a result of vasoconstriction.
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PMID:Lewy bodies in the sinoatrial nodal ganglion: clinicopathological studies. 1536 36

SummaryConcern about long-term complications after intraatrial repair of complete transposition has been used as an argument in favor of "anatomic" repair by the arterial switch operation. Late arrhythmias, including loss of sinus rhythm and the development of supraventricular tachycardias, particularly atrial flutter, are widely reported after intraatrial repair. Despite modifications of technique, the electrophysiologic substrate for arrhythmia results from the extensive atrial surgery required. Arrhythmias occur, even in the "modern surgical era" after both Mustard and Senning operations, are progressive, and appear to be inevitable. The circulation after an intraatrial repair is more vulnerable to the effects of excessive tachycardia, and this may place the patient at risk from sudden cardiac death. Current attempts at individual stratification of risk are disappointing using even aggressive electrophysiologic approaches, and a combined assessment involving hemodynamics is likely to be necessary. The electrophysiologic and arrhythmic consequences of the arterial switch operation have been less extensively researched but, as might be expected, are quite different from those seen after intraatrial repair. The atrial activation sequence is relatively undisturbed, and sinus nodal dysfunction and supraventricular arrhythmia are uncommon. Ventricular extrasystoles are the arrhythmia most consistently found during the short follow-up currently available. In the longer term, myocardial ischemia, hemodynamic disturbances and autonomic imbalance may predispose to late arrhythmia. Current evidence would suggest that the lack of clinically significant arrhythmia and the restoration of the left ventricle to the systemic circulation are significant advantages of the arterial switch operation over intraatrial repair procedures.
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PMID:Arrhythmias after surgery for complete transposition: Do they matter? 2111 87

Cellular metabolism and reactive oxygen species (ROS) formation are interrelated processes in mitochondria and are implicated in a variety of human diseases including ischemic heart disease. During ischemia, mitochondrial respiration rates fall. Though seemingly paradoxical, reduced respiration has been observed to be cardioprotective due in part to reduced generation of ROS. Enhanced myocardial glucose uptake is considered beneficial for the myocardium under stress, as glucose is the primary substrate to support anaerobic metabolism. Thus, inhibition of mitochondrial respiration and uncoupling oxidative phosphorylation can protect the myocardium from irreversible ischemic damage. Growing evidence now positions the TXNIP/thioredoxin system at a nodal point linking pathways of antioxidant defense, cell survival, and energy metabolism. This emerging picture reveals TXNIP's function as a regulator of glucose homeostasis and may prove central to regulation of mitochondrial function during ischemia. In this review, we summarize how TXNIP and its binding partner thioredoxin act as regulators of mitochondrial metabolism. While the precise mechanism remains incompletely defined, the TXNIP-thioredoxin interaction has the potential to affect signaling that regulates mitochondrial bioenergetics and respiratory function with potential cardioprotection against ischemic injury.
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PMID:Thioredoxin-interacting protein and myocardial mitochondrial function in ischemia-reperfusion injury. 2389 54


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