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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic preconditioning (PC) has been shown to limit ischemia- and reperfusion-induced arrhythmias. We wished to determine whether the antiarrhythmic effect of PC would be affected by inhibition of the L-arginine nitric oxide (NO) pathway in anesthetized rats. Ischemia and reperfusion were produced by occlusion and release of a snare around the left coronary artery in all rats. The effect of PC (three cycles of 2-min coronary artery occlusion and 5-min reperfusion) on development of reperfusion-induced arrhythmias after 5-min coronary artery occlusion was studied in 12 rats. In 24 other rats, the specific NO synthesis inhibitor NG-monomethyl-L-arginine (L-NMMA 10 mg/kg, n = 12) or the muscarinic receptor antagonist-NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME 10 mg/kg, n = 12), was administered intravenously (i.v.) before PC. In control groups, solvent (n = 15), L-NAME (10 mg/kg i.v., n = 12), L-NMMA (10 mg/kg i.v., n = 12), or L-arginine (L-Arg 100 mg/kg i.v., n = 12) was administered to rats 5 min before coronary artery occlusion without PC. PC significantly reduced the incidence of ventricular premature beats (VPBs) from 100% in the non-PC solvent group to 17%, decreased the incidence of ventricular tachycardia (VT) from 93 to 8%, and abolished the incidence of reversible and irreversible ventricular fibrillation (RVF and IVF: 87 and 47% in the non-PC solvent group, respectively). L-NAME and L-NMMA did not significantly affect the protective effect of PC on reperfusion-induced arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does the antiarrhythmic effect of ischemic preconditioning in rats involve the L-arginine nitric oxide pathway? 759 18

For many years ischemic heart disease involving the right ventricle had received little attention. During the last 15 years, the initial works of Cohn, Isner, and others spawned a number of clinical and experimental studies that extended the understanding of the pathophysiology of ischemia in the right ventricle. Most of the work has been done in the setting of acute myocardial infarction, and information is still lacking in other conditions, such as chronic ischemic heart disease and perioperative right ventricular dysfunction. Acute right ventricular infarction rarely occurs in the absence of left ventricular necrosis and in most cases is the extension of an inferior left ventricular infarct. The majority of patients with right ventricular infarction only exhibit subtle signs of ischemic dysfunction. Elevated right atrial pressure is found only in the typical syndrome of elevated venous pressure; low output syndrome can be found only in 20% of the cases, and cardiogenic shock secondary to right ventricular necrosis is found only in 10%. It is also important to note that there is not a clear correlation between the severity of ischemic right ventricular dysfunction and the necrotic area. The discrepancy may be due to ischemia without necrosis of the right ventricular wall (stunned myocardium), but the intact pericardium and the necrosis of the interventricular septum may also play an important role. In the most severe form of ischemic right ventricular dysfunction, the entire right ventricular wall is akinetic. Right atrial, right ventricular, and pulmonary artery pressures become similar in magnitude and shape, and the pulmonary valve is opened during diastole, demonstrating a passive blood flow from the right atrium to the left ventricle through the low resistance pulmonary capillary bed. Volume loading, administration of dopamine or dobutamine, and careful use of vasodilators under hemodynamic monitoring are the therapeutic measures to control the severe forms of acute ischemic right ventricular dysfunction. The use of thrombolytic agents has decreased the incidence of right ventricular dysfunction after acute myocardial infarction. Mortality is high in the severe forms of acute ischemic right ventricular dysfunction, but after discharge from hospital the prognosis is good and right heart failure is unusual, even in those patients with shock during the first days of evolution of the infarct.
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PMID:Ischemia right ventricular dysfunction. 794 82

The human right ventricle has a relatively low tolerance to even short periods of ischemia. During angioplasty of the right coronary artery, pulmonary artery pressure typically rises due to an increase in right ventricular afterload caused by left ventricular dysfunction during ischemia. We have presented two cases of angioplasty in the early proximal portion of a large, highly dominant right coronary artery. Pulmonary artery and systemic pressure fell during balloon inflation probably secondary to acute severe right ventricular failure, though an interaction with left ventricular dysfunction cannot be excluded. These observations do emphasize the hemodynamic and combined ventricular consequences of proximal angioplasty in a large, dominant right coronary artery, particularly in the setting of preexisting left ventricular dysfunction.
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PMID:Pulmonary artery hemodynamic response to proximal balloon dilatation of a large dominant right coronary artery. 822 55

Early cardiac graft failure has been reported to occur in 4-25% of patients undergoing orthotopic heart transplantation. To further elucidate the characteristics and prognosis of patients with graft failure, we retrospectively identified 10 patients from a series of 212 consecutive recipients with catastrophic graft dysfunction in the absence of acute cellular rejection, right ventricular failure secondary to pulmonary hypertension and technical factors. We present a case report and the experience from one transplant center, a review of the literature and possible strategies for the management of early graft failure. Mean onset of graft failure was 6.5 days (range intraoperative to 23 days). Multivariable analysis revealed a longer total ischemic time in patients with early graft dysfunction (200 +/- 14 vs. 166 +/- 4 min). No episodes of hyperacute rejection were observed. Pathologic changes noted on biopsy or autopsy included ischemia in 9 and vascular rejection in 1. The mortality at 60 days was 50%. Early use of aggressive mechanical and pharmacological support is described and appears to be important for graft salvage.
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PMID:Early cardiac allograft failure after orthotopic heart transplantation. 827 37

Right ventricular cardiac function is altered by abnormalities affecting primarily the left-sided cardiac structures, the lungs, or the right-sided cardiac structures themselves. The most common cardiac causes for right ventricular dysfunction are chronic left ventricular ischemia and rheumatic mitral valvular disease. Pulmonary diseases that result in right ventricular dysfunction include pulmonary air-space disease, including emphysema, and pulmonary interstitial and parenchymal diseases, including idiopathic pulmonary fibrosis and cystic fibrosis. Chronic pulmonary vascular disease, including chronic thromboembolism and PPH have a significant effect on right ventricular performance. Common to all of these diseases is elevation of pulmonary vascular resistance with a commensurate increase in right ventricular pressure, resulting in right ventricular hypertrophy. The limited ability of right ventricular myocardium to function in the face of increased pulmonary resistance results in right ventricular dilatation, tricuspid regurgitation, and ultimately right ventricular failure. MR imaging provides direct, noninvasive visualization of the right ventricular chamber as well as the myocardium itself, allowing reliable demonstration of morphologic changes in the size and shape of the ventricle, thickness of the myocardium, and presence of abnormal infiltration by fat or edema. Furthermore, because MR imaging techniques do not depend upon geometric assumptions about the complex shape of the right ventricle, they may be used for accurate and reproducible quantitation of right ventricular volume and myocardial mass.
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PMID:MR imaging of pulmonary hypertension and right ventricular dysfunction. 872 68

The two primary goals of mechanical circulatory support are to provide adequate perfusion of the vital organs and to decrease cardiac work. The support of the myocardium is in an effort to cause a reversal of cardiac damage. The recovery process apparently takes place in two stages. Initially, there is a rapid functional recovery of cells in marginally ischemia areas. Then there is a slower process of hypertrophy of normal and recovering myofibers. The process involves the reversal of interstitial and of intercellular myocardial edema in areas of viable myocardium while halting the extension of necrosis into reversibly ischemic areas. It appears that this process is extended from 3 to 5 days, and functional recovery can occur for up to 2 weeks. After a 2-week period, there appears to be little functional recovery of myocardial cells. In autopsy series of nonsurvivors, it appears that most of the patients had suffered from biventricular failure. Biventricular failure appears to be one of the more common complications of the support patient. Right ventricular failure will be attempted to be supported by right ventricular assist devices. The right ventricular assist device, unfortunately, adds a level of complication to the recovery process for the bridge-to-transplant or cardiomyopathy patient. The patients who are involved in support fall into three categories: (1) the bridge-to-transplant patient, (2) the patient recovering from postcardiotomy, and (3) the patient who recovers from an acute myocardial insult. It appears that after 2 weeks the recovery period for all of these groups demonstrates no further functional recovery. The bridge-to-transplant patients usually need to be supported until the transplant occurs. The postcardiotomy patient and the acute myocardial failure patient are the most disappointing support group, since they have a higher morbidity and mortality, and a lower chance of recovery. Salvage rates appear to be in approximately the 25% range in the acute insult category.
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PMID:Cardiac assist devices. 879 47

To present an overview of the surgical issues in lung transplantation, including the historical context and the rationale for choosing a particular procedure for a specific patient, we reviewed and summarized the current medical literature and our personal experience. Several surgical options are available, including single lung transplantation; double lung transplantation; heart-lung transplantation; bilateral, sequential single lung transplantation; and (recently) single lobe transplantation. Although single lung transplantation is preferred for maximal use of the available organs, bilateral lung transplantation is necessary for septic lung diseases and may be appropriate for pulmonary hypertension and bullous emphysema. Heart-lung transplantation is performed for Eisenmenger's syndrome and for primary pulmonary hypertension with severe right ventricular failure. General factors for consideration in assessment of compatibility of the donor and potential recipient include ABO blood group, height (the donor should be within +/- 20% of the recipient's height), and length of the lungs (determined on an anteroposterior chest roentgenogram). Graft preservation and minimal duration of ischemia are important. Complications associated with airway healing are related to ischemia of the donor bronchus. We have addressed the issue of donor bronchial ischemia by direct revascularization of the donor bronchial arteries with use of the recipient's internal thoracic artery. Currently, lung transplantation offers a realistic therapeutic option to patients with end-stage pulmonary parenchymal or vascular disease.
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PMID:Surgical issues in lung transplantation: options, donor selection, graft preservation, and airway healing. 900 92

Mechanical assisted circulation by the means of cardiac assist devices is a routine procedure in modern cardiac surgery and cardiology. We investigated the impact of mechanical unloading on regional myocardial "stunning" and the influence of assisted circulation on left heart and right heart failure persevered by an ultimate addition of pulmonary hypertension in experimental set ups. We found that mechanical unloading either during ischemia or in the early reperfusion phase attenuates stunning and enhances the return of synchronous heart performance. In our global dysfunction model we showed that the right heart is dispensable. Sufficient inflow to the left heart is provided unless pulmonary hypertension is present. Also additional left heart support can not overcome the deleterious situation and in select cases only additional right heart support can prevent the "low LVAD output" syndrome. We conclude that mechanical assisted circulation and mechanical unloading are beneficial in case of regional and global dysfunction persevered by pulmonary hypertension, however, the knowledge about interactions of assist systems and the circulation has to be improved in order to optimize clinical assist device performance.
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PMID:Pathophysiological considerations concerning uni- and biventricular mechanical cardiac assist. 950 83

The present review is focused on chronic RV pressure overload or Cor Pulmonale as it may occur in the setting of two distinct disorders: those associated with abnormal pulmonary gas exchange (hypoxemia and/or hypercapnia) where chronic obstructive pulmonary disease (COPD) is the leading cause, and those associated with pulmonary vascular obstruction where primary pulmonary hypertension (PDDH) is the representative example. The clinical curse, prognostic, implications, and therapeutic strategies differ considerably in these two clinical entities. Right ventricular failure (RVF) may adversely influence the natural history and prognosis of patients with diverse cardiopulmonary disorders. It has been long established that right ventricular (RV) ischemia, RV overload, and RV pressure overload, alone or in combination, are the main factors involved in the pathogenesis of RVF. From the pathophysiologic point of view, RVF of COPD is more a congestive type of failure, in which activation of renin-angiotensin system is involved. In PPH, a low cardiac output state is predominant and the precise mechanism of RVF remains unknown. Current evidence in favor of the pathogenetic role of ischemia, adrenergic overdrive, and genetic determination are all reviewed during the course.
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PMID:[Right ventricle insufficiency in pulmonary arterial hypertension. Physiopathologic considerations]. 1156 26

Acute right ventricular ischemia accompanies 40-80% of cases of infero-posterior myocardial infarction. Approximately one half of these patients present with hemodynamic compromise consisting of acute right ventricular failure, clear lungs and low cardiac output in spite of preserved left ventricular systolic function. The ischemic right ventricle appears to be relatively resistant to infarction and has remarkable ability to recover. Right ventricular performance improves spontaneously even in the absence of reperfusion, however reperfusion enhances this recovery and improves the clinical course of right ventricular infarction.
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PMID:[Right ventricular infarction: pathophysiology, diagnosis and treatment]. 1251 44


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