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Query: UMLS:C0034065 (pulmonary embolism)
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Ventricular dysfunction, then, does indeed occur during liver transplantation, particularly at the time of reperfusion. Pulmonary embolism contributes to right ventricular and right atrial encroachment on left-heart filling, and paradoxical embolism may occur. Pericardial effusions, tricuspid regurgitation, hypothermia, and the release of substances, particularly potassium from the donor liver, may further contribute to compromises in ventricular function. Proper monitoring and appropriate treatment, however, lead to successful operative outcomes in most cases.
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PMID:Ventricular dysfunction does occur during liver transplantation. 206 29

To define the mechanisms of unexpected cardiac arrest in advanced heart failure, we reviewed the causes of cardiac arrest as established from electrocardiographic monitoring and from clinical and autopsy data in patients hospitalized for cardiac transplantation evaluation and management of advanced heart failure (mean left ventricular ejection fraction, 0.18 +/- 0.08) who were stable while on vasodilator and diuretic therapy such that hospital discharge to home was anticipated. Twenty-one cardiac arrests occurred in 20 of 216 (9%) such patients during a 4-year period. Heart failure was due to coronary artery disease with prior myocardial infarction in 13 patients and nonischemic cardiomyopathy in seven patients. The rhythm at the time of arrest was severe bradycardia or electromechanical dissociation (BA/EMD) in 13 (62%) patients. The precipitating cause of the BA/EMD arrest was coronary artery thrombosis or embolism in two patients, pulmonary embolism in one patient, hyperkalemia in two patients, and unexplained hypoglycemia in one patient. In seven of 13 (54%) patients, a precipitating cause of the bradycardia arrest could not be established. Only eight of 21 (38%) arrests were due to ventricular tachycardia or fibrillation (VT/VF), and all occurred in patients with prior myocardial infarction (p = 0.02 vs. BA/EMD arrests). Two VT/VF arrests were due to acute or recent infarction, and one patient had hyperkalemia. The patients who suffered a BA/EMD arrest were similar to those who had a VT/VF arrest in age, ventricular arrhythmia history, ventricular function, and serum potassium levels. Serum sodium levels were lower in patients with BA/EMD arrests (129 +/- 3 vs. 133 +/- 4 meq/l, p = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diverse mechanisms of unexpected cardiac arrest in advanced heart failure. 259 30

To determine if the addition of potassium enhances the myocardial protective effect of intracoronary perfusion hypothermia during aortic cross-clamping, 50 patients undergoing aortocoronary bypass grafting were studied in a randomized, prospective, double-blind fashion. Twenty-six patients received a cold crystalloid solution infused with a handheld syringe into the root of the cross-clamped aorta every 20 minutes, and 24 patients received the same solution but with 25 mEq/L of potassium chloride added, infused in a similar manner. Both groups were analyzed by mortality, rate of perioperative myocardial infarction (electrocardiographic changes, MB-CPK enzyme release, and preoperative and postoperative gated cardiac blood pool scans), intraoperative hemodynamic changes, intraoperative lactate determinations, postoperative arrhythmias, and requirement for pressor or intraaortic balloon pump support. One patient in the potassium cardioplegia group died (massive pulmonary embolism), and none in the hypothermic perfusion group died. Possible perioperative myocardial infarction was diagnosed by more than one marker in 4 of 26 patients in the hypothermic perfusion group and 5 of 24 patients in the potassium group (p = 0.61). There were no differences between the two groups in terms of hemodynamic changes, lactate production, postoperative arrhythmias, or the need for postoperative hemodynamic support. This study in human beings could not demonstrate a specific protective effect of potassium, beyond that afforded by myocardial perfusion hypothermia and wash-out. The data suggest that myocardial hypothermia, achieved through cold intracoronary arterial perfusion, may be the most important beneficial component of so-called cardioplegia for attaining effective intraoperative myocardial preservation in human beings.
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PMID:Hypothermic ischemic arrest versus hypothermic potassium cardioplegia in human beings. 704 99

We report a case of renal vein thrombosis (RVT) and pulmonary embolism associated with diffuse membranous glomerulonephritis. A 44-year-old Japanese male was referred to the Nephrology Department with heavy proteinuria. Renal biopsy revealed diffuse membranous glomerulonephritis and we administered PSL 30mg/day and dipyridamole 300mg/day. Three weeks later, he was admitted with severe chest pain, dyspnea and massive proteinuria. RVT and pulmonary embolism were detected on CT scan and perfusion lung scan. After a few days of continuous intravenous unfractionated heparin (UFH) therapy, we used 72 U (anti-FXa)/kg of intravenous low-molecular-weight heparin (LMWH) every 12 hours for 10 days. He also received urokinase at the dose of 120,000 U/day for 4 weeks and long-term therapy with warfarin potassium at the dose of 3 mg/day. One month later, the thrombi in the pulmonary arteries and inferior vena cava disappeared on CT scan and perfusion lung scan. LMWHs have a longer biological half-life and a lower bleeding tendency than UFH for an equivalent antithrombotic effect. This case indicates that intermittent intravenous LMWH administration combined with urokinase is effective against RVT and pulmonary embolism without any side effect.
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PMID:[A case of renal vein thrombosis and pulmonary embolism associated with diffuse membranous glomerulonephritis: the usefulness of low-molecular-weight heparin and urokinase therapy]. 769 54

Protection of the failing right ventricle (RV) in the surgical treatment of massive pulmonary embolism is a keystone for myocardial recovery. This study evaluated whether cardioplegia should be used or avoided. In a modified Langendorff rat heart model pulmonary embolism was simulated by afterload elevation (20 cm H2O) for 30 min. Hearts were arrested with cardioplegic solutions [St. Thomas Hospital (ST); University of Wisconsin (UW); oxygenated Krebs-Henseleit-Potassium (KHP)] and stored for 10 min or were allowed to beat empty (NoCP) for 15 min. After reestablishing of baseline conditions groups were measured for 60 min. Cardiac index (CI) decreased in all groups to 20% during afterload elevation. Group NoCP showed 68 and Group ST 65% recovery after 10 min and deteriorated after 30 min. After 60 min CI was 37 (ST) and 39% (NoCP). UW and KHP showed a significantly better recovery (KHP 100%; UW 88%). At 60 min CI decreased to 60 (KHP) and 64% (UW), but was still significantly higher than corresponding values of NoCP and ST. Following increased pulmonary afterload cardioplegia with UW or KHP solution is beneficial for RV recovery. The composition of the cardioplegia is obviously important and needs further study.
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PMID:Protection of the right ventricular myocardium during acute right heart failure from pulmonary hypertension. 813 48

The aim of this study was to evaluate the action of trandolapril on blood glucose control and microalbuminuria in mild to moderate hypertensive in patients with non-insulin-dependent diabetes. Sixty-seven patients, aged between 33 and 79, were enrolled. After a two week placebo run-in period, treatment with trandolapril as monotherapy was given for 3 months. The dose of trandolapril was adjusted between 1 and 4 mg/day according to antihypertensive response. Patients were assessed clinically and by laboratory investigations each month. Two patients were excluded from efficacy analysis because of major protocol deviations. Mean DBP fell, under the influence of treatment, from 101 +/- 5 mmHg to 82 +/- 7 mmHg (p < 0.0001) and mean SBP from 171 +/- 9 mmHg tp 147 +/- 11 mmHG (p < 0.0001). At three months, 54 patients (84%) had a DBP < or = 90 mmHg. Microalbuminuria decreased significantly (p = 0.03) during treatment. Microalbuminuria returned to normal in 11 of the 13 patients in whom the baseline value was above 21 micrograms/min and increased to above normal in 2 of the 26 patients who had a normal baseline value. Blood glycosylated hemoglobin, fructosamine, glucose and creatinine, and creatinine clearance remained stable. Plasma potassium rose slightly in 7 patients. Six adverse events were reported (4 coughs, 1 peripheral edema, 1 plantar mal perforans). One patient died from pulmonary embolism. In conclusion, trandolapril is an effective antihypertensive agent in hypertensive diabetics. Trandolapril causes a significant decrease in microalbuminuria and does not interfere with blood glucose control in these patients.
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PMID:[Action of trandolapril on the blood glucose balance and microalbuminuria in hypertensive diabetics]. 817 83

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

A 68-year-old woman was admitted to our hospital due to brain embolism in the right middle cerebral artery. Patent foramen ovale was detected by transesophageal echocardiogram. The sonogram of the legs revealed a floating thrombus originating from the left posterior tibial vein and extended to the superficial femoral vein. Both right middle lobe and left upper lobe were defected in perfusion scans of lung. She was treated with administration of warfarin potassium and caval filters placed in the inferior vena cava and the azygos vein. Thereafter, she had never experienced brain embolism or pulmonary embolism. A floating deep venous thrombus, which is a high risk of pulmonary embolism, could be observed in patients with paradoxical brain embolism. It was suggested that sonography of veins in the legs is essential for detecting embolic sources of brain infarction, as well as evaluating the risk of pulmonary embolism.
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PMID:[Paradoxical brain embolism with a floating deep venous thrombus detected by sonography of lower extremities]. 1591 4

The T-wave of the electrocardiogram (ECG) is generated both from the left and the right ventricles of the heart. Each ventricle may produce a normal, an "ischemic", or a "secondary" T-wave, depending on segmental perfusion, intraventricular pressure, or QRS complex duration. The direction of the T-wave is determined by the particular inward rectifier potassium channels recruited by various layers and segments in the two ventricles. The observed T-wave in the clinical ECG is the summation of the left and right ventricular T waves, and is thus biventricular. Clinical observations in right bundle branch block (RBBB) and in right ventricular hypertensive states such as pulmonary embolism suggest that many ECG's interpreted as inferior or anterior left ventricular ischemia are in fact examples of abnormal potassium channel recruitment in the right ventricle. Consideration of the right ventricular component of the T-wave in every electrocardiographic interpretation improves diagnostic understanding and accuracy, as the possible right ventricular origin of observed anterior or superior T waves will not be overlooked.
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PMID:T waves are independently generated in both right and left ventricles: the clinically recorded T is a summation of two separate repolarizations, and is thus always biventricular. 1608 69

An 85-year-old lady with type 2 diabetes mellitus of 32 years duration with peripheral neuropathy was admitted under the vascular surgeons with extensive gangrene of her lower limb. She was on insulin for the last 7 years. Initial investigations showed normal serum electrolytes. She was started on antibiotics and unfractionated heparin, and her electrolytes showed hyperkalemia, which persisted on active treatment. Her short synacthen test showed good response, renin was normal with low aldosterone, urinary pH, sodium, potassium and osmolality was normal. On stopping heparin serum, potassium became normal. On restarting heparin (low molecular weight) during a suspected episode of pulmonary embolism, she developed hyperkalemia and heparin was stopped. Her potassium and aldosterone became normal on discontinuation of heparin. She developed hyperkalemia with both unfractionated and low molecular weight heparin.
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PMID:Heparin-induced hyperkalemia. 1834 25


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