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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

William Heberden (1710--1801), in 1768, described angina pectoris, the classic symptom of ischemic heart disease, 150 years after the discovery of the coronary circulation by William Harvey (1578-1657). Another 110 years had elapsed before the first antemortem diagnosis (confirmed at autopsy) of coronary thrombosis was reported by Adam Hammer in 1878. The patient was a 34 year old man who died some 19 hours after a sudden collapse. Although the patient's clinical features were atypical (such as the absence of angina and the presence of complete heart block) and the autopsy showed vegetative aortic endocarditis that appeared to be causally related to the thrombotic coronary occlusion, Hammer's astute and carefully reasoned bedside diagnosis was history-making and deserves to be so recognized.
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PMID:Centenary of the first correct antemortem diagnosis of coronary thrombosis by Adam Hammer (1818--1878): English translation of the original report. 36 Aug 11

Inadequate left internal mammary artery (LIMA) graft to the left anterior descending artery (LAD) was encountered in 10 of 3,076 patients between 1984 and July 1990. The mean number of bypass grafts was 2.9 per patient. All patients with inadequate LIMA grafts were stable preoperatively with normal to moderately reduced left ventricular function. No technical difficulties were encountered during surgery. All patients were weaned off cardiopulmonary bypass with minimal or no inotropic support. Each patient developed myocardial ischemia of the LAD territory and/or circulatory collapse or recurrent ventricular dysrhythmia during the first 24 h postoperatively. Six patients, who were immediately re-operated on and had an additional saphenous graft to the LAD, recovered with no infarction and good functional results. Four patients, who were medically treated, developed myocardial infarction. In cases of refractory circulatory collapse and/or ventricular dysrhythmia, inadequate LIMA flow should be suspected. We recommend urgent re-operation with additional saphenous vein graft to the LAD.
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PMID:Inadequate internal mammary artery graft as a cause of postoperative ischemia: incidence, diagnosis and management. 136 Feb 22

The combination of different ultrasound techniques like transthoracic, suprasternal, subcostal and transesophageal echocardiography have a high sensitivity and specificity in the diagnosis of aortic dissection. The limitation of this combined ultrasound technique is related to the visualization of the ascending part of the aortic arch which, cause of the interposition of the trachea, can not be visualized completely. The beginning or the end of a dissection in this part of the aorta may be misinterpreted. False negative results are rare. False positive results due to artefacts resulting from reverberations in an ectatic ascending aorta have to be taken into account. The most important diagnostic aims in acute or chronic aortic dissection can be described: 1. confirmation of the diagnosis by visualization of the intima membrane, 2. the differentiation of the true and false lumen depending on visualization of spontaneous echocardiographic contrast thrombus formation, slow or reduced reversed flow, systolic diameter reduction and signs of entry jet into the false lumen, 3. detection of intimal tear, demonstrating communication by two-dimensional or color Doppler echocardiography, 4. determination of the extent of the dissection with classification according to DeBakey type I, II and III or Stanford A and B with differentiation to communicating or non-communicating dissection, antegrade or retrograde dissection limited to the descending aorta or expanding to the ascending aorta, 5. detection of wall motion abnormalities as a sign of preexisting coronary artery disease or myocardial ischemia due to ostium occlusion by an intimal flap, coronary artery rupture or collapse of the true lumen during diastole, 6. detection and grading of aortic insufficiency, 7. detection of side branch involvement by suprasternal, subcostal and abdominal sonography, which will gain the information which side can be chosen for cannulation or catheterization at the femoral artery, 8. detection of pericardial pleural effusion and mediastinal hematoma as a sign of emergency as rupture can occur within minutes. Without surgical intervention have be performed. Based on these informations, surgery can be performed in all acute situations in type A dissection without further investigations. This decision is particularly important in patients with signs of emergency like pericardial or pleural effusion or mediastinal hematoma.
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PMID:[Diagnostic goals in aortic dissection. Value of transthoracic and transesophageal echocardiography]. 148 22

Although both asymptomatic ventricular arrhythmias and sudden death are common in patients with chronic heart failure, there is little evidence that patients who have frequent or complex ventricular arrhythmias are at increased risk of sudden death. Two hypotheses may explain the lack of an arrhythmia-sudden death relation in this disorder. First, complex ventricular arrhythmias may be a nonspecific manifestation of a dying left ventricle rather than an indication of a specific arrhythmogenic substrate. In fact, during long-term follow-up, patients with mild heart failure who have nonsustained ventricular tachycardia are more likely to develop clinical progression of the disease rather than sudden death. Second, sudden death may be related to events other than a malignant ventricular arrhythmia. The most common myocardial ischemia, whereas the terminal event in patients with an idiopathic dilated cardiomyopathy is commonly a severe bradyarrhythmia or electromechanical dissociation. Neither outcome can be predicted by a prior history of ventricular arrhythmias on ambulatory electrocardiographic monitoring. If asymptomatic ventricular arrhythmias do not lead to sudden death, then there would appear to be little reason to expect that antiarrhythmic drugs could prevent cardiac arrest in patients with chronic heart failure. This may explain why drugs that suppress ambulatory arrhythmias do not prevent sudden death in these patients, whereas interventions may reduce the risk of unexpected circulatory collapse in this disorder without suppressing ventricular ectopic activity. To make matters more complicated, the desirable actions of antiarrhythmic drugs are attenuated and their negative inotropic and proarrhythmic actions are enhanced in patients with severe cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of relation between ventricular arrhythmias and sudden death in patients with chronic heart failure. 172 5

Left atrial booster pump function produces variable effects on cardiac output. Generally, cardiac output decreases by only 15-20% when atrial fibrillation occurs, however, in some cases, hemodynamic collapse occurs through loss of left atrial contraction. We evaluated the relative significance of left atrial booster pump function in acute or chronic load and in myocardial ischemia using the left ventricular volume curve. Blood entering into the left ventricle during the left atrial contraction phase (FVLA) represents the left atrial volume work, and the ratio of FVLA to the left ventricular filling volume during one cardiac cycle (%FVLA) represents the relative significance of left atrial booster pump function in cardiac output. In dog experiments, we calculated the change in FVLA and %FVLA by measuring the the left ventricular internal minor axis diameter and using Pombo's method. We also measured the change of the left atrial segment length as a direct indicator of left atrial contraction. In the acute change in preload, FVLA changed with stroke volume, but %FVLA remained unchanged. The change in FVLA correlated with the direct indicator of the left atrial excursion; the extent of the left atrial segment length (LASL). During acute change of left ventricular afterload, both FVLA and %FVLA were unchanged. In regional myocardial ischemia, both FVLA and %FVLA were increased, suggesting an increase in the left atrial booster pump function. In clinical study, we calculated FVLA and %FVLA from the left ventricular diameter using M-mode echocardiography. In chronic volume overloading (aortic regurgitation), FVLA increased while %FVLA was maintained unchanged. The same FVLA-%FVLA relationship was observed in acute volume loading. In cases of left ventricular hypertrophy (LVH) and old myocardial infarction (MI), both FVLA and %FVLA were increased, suggesting the increased left atrial booster pump function. In these cases, the left ventricular rapid filling velocity decreased, suggesting that impairment of rapid filling caused the increase of left atrial preload and hence increased left atrial volume work. The results of this study show that in old MI and in LVH, both left atrial volume work and the relative significance of left atrial booster pump function increase. We concluded that prevention of atrial fibrillation may be very important in these diseases.
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PMID:[Left atrial booster pump function in left ventricular blood filling: clinical and experimental analyses]. 184 34

To determine whether myocardial dysfunction contributes to vascular collapse in anaphylactic shock, we examined left ventricular (LV) contractility, coronary blood flow, and myocardial lactate metabolism during antigen challenge in eight dogs that were sensitized to ragweed pollen extract (anaphylaxis group). Findings in the anaphylaxis group were contrasted to those in another group of dogs in which mean blood pressure was decreased to the same extent by arteriolar vasodilation with nitroprusside. The animals were examined under nonhypoxic conditions while anesthetized and ventilated. LV mechanics were examined with subendocardial crystals placed primarily along the anterior-posterior minor axis of the LV. During antigen challenge, a depression in LV contractility was observed in the anaphylaxis group as assessed by fractional dimensional shortening, stroke volume, and the slope of the end-systolic pressure-dimension relationship. During anaphylaxis, moreover, coronary vasodilation rather than coronary vasoconstriction was observed, and evidence of myocardial ischemia as assessed by altered myocardial lactate metabolism was not found. Our results indicate that depressed LV contractility occurs in anaphylactic shock. The results further suggest that the mechanism may be due to a direct effect of mediators of anaphylaxis on the myocardium to produce systolic dysfunction.
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PMID:Left ventricular contractility is depressed in IgE-mediated anaphylactic shock in dogs. 200 Sep 70

The OSA syndrome, described over 100 years ago, was rediscovered in 1966. It is a common disorder, especially among fat, middle-aged men. Stentorian snoring and diurnal somnolence are the cardinal manifestations and should always lead to an examination during sleep. That examination (polysomnography) can demonstrate the pathognomonic events--repetitive apneas occurring in sleep--which signal the failure of the sleeping brain to maintain the patency of the supraglottic airway. All evidence points to the problem being an abnormal pharyngeal airway, one which has a shape or size or compliance that allows inspiratory collapse as the normal loss of pharyngeal dilator muscle tone occurs with sleep. The apneas are asphyxic events terminated by arousals which fragment sleep continuity and lead to the daytime sleepiness. Because the snoring occurs during sleep, the arousals are unremembered, and the sleepiness can develop so gradually that the patient may forget what normal alertness is like. It is important to interview the patient's spouse or partner. Besides obesity and maleness, other risk factors for OSA are diseases that have an impact on the configuration or effective compliance of the pharyngeal passageway. Recent studies support the clinical intuition that sleep apnea is undesirable. Sleepiness leads to accidents. The hypoxemia occurring during apnea can lead to potentially fatal cardiac dysrhythmias. A number of reports suggest that snoring and sleep apnea are associated with an increased risk of stroke, myocardial ischemia, and infarction. Finally, there are now two papers showing a significantly decreased probability of 5-year survival in patients with symptomatic sleep apnea. The good news is that treatment with tracheostomy or NCPAP improves mortality rates to normal. Approximately 90 per cent of patients can tolerate a night's initial trial with CPAP. Long-term acceptance of CPAP has now been reviewed in a number of studies, and it appears to be about 65 to 70 per cent.
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PMID:Sleep disorders and upper airway obstruction in adults. 219 4

An anaphylactic reaction in the isolated perfused heart is characterized by a drastic coronary constriction, arrhythmias, and an impairment of contractility. In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to ascertain the electrocardiographic and cardiovascular changes during systemic hypersensitivity reactions. In addition, an attempt was made to differentiate cardiac from respiratory events. In guinea pigs, sensitization was produced by s.c. administration of ovalbumin together with Freund's adjuvant solution. Fourteen days after sensitization, the effects of an i.v. infusion of ovalbumin were tested in the anesthetized guinea pigs, which were ventilated with room air or 100% oxygen. A second administration of the antigen induced the development of cardiovascular collapse, leading to death within 12 min. Within 3 min, cardiac output decreased by 90% and end-diastolic left ventricular pressure increased significantly, indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, arrhythmias occurred in the form of atrioventricular block. Left ventricular contractility declined continuously within the first 4 min. Finally, after 4 min, blood pressure steadily decreased. During ventilation with room air, severe hypoxia developed, with arterial PO2 decreasing from 94 mmHg to 14 mmHg after 3 min. However, under ventilation with 100% oxygen, a dissociation between cardiac damage and respiratory distress occurred. Myocardial ischemia and signs of cardiac failure preceded the development of hypoxia by a significant time interval. It is to be concluded that cardiac damage is a primary event in anaphylactic shock. Furthermore, the electrocardiographic signs of ischemia are interpreted as a result of coronary artery spasm.
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PMID:Systemic anaphylaxis--separation of cardiac reactions from respiratory and peripheral vascular events. 221 74

Evidence exists that many of the victims of cardiac arrest due to ischemic heart disease can be resuscitated if cardiopulmonary resuscitation (CPR) and defibrillation are made available in the minutes following collapse. In order to evaluate the ability of the general public in Dublin to perform CPR appropriately, 225 people were asked when CPR was indicated and how cardiac arrest was diagnosed and then asked to perform CPR on a mannequin. In the knowledge sections, 45% gave an appropriate indication for CPR and 34% gave appropriate criteria for diagnosing cardiac arrest. However, only eight participants were able to perform CPR correctly and only six (2.6%) had both the correct skills and knowledge. There is an urgent need to improve the public's knowledge of and ability to perform CPR as part of an overall strategy to decrease mortality from ischemic heart disease in Ireland.
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PMID:Resuscitation skills among the general public in Dublin. 222 35

The long-term prognosis for 314 patients with hypertrophic cardiomyopathy (HCM) and 82 with dilated cardiomyopathy (DCM) was investigated in an attempt to elucidate clinical variables predicting sudden death (SD). In the patients with HCM, 68% of cardiac deaths occurred suddenly and unexpectedly. Variables associated with an increased risk to SD were young age (less than 30 years), reduced fractional shortening (less than 35%) and elevated left ventricular end-diastolic pressure (greater than or equal to 20 mmHg). Eight of the 10 patients who died suddenly during or immediately after strenuous exercise were less than 30 years old, and the collapse tended to be associated with exercise-induced ST-depression. In contrast, SD occurring during mild activities, resting or sleep was mainly observed in those aged 30 years or more. Ventricular tachycardia was observed on electrocardiographic monitoring in 24% of those 30 years or more, while it was rare in those under 30 years (5%). On the other hand, no SD was found in patients with apical hypertrophy nor in those 50 years or more. These observations suggest that HCM patients at a young age, with impaired left ventricular systolic and diastolic function, have an increased risk to SD. Since exercise-induced myocardial ischemia rather than ventricular arrhythmias appears to be the more likely mechanism for SD for those under 30 years old, restriction of strenuous exercise should be strongly advised for these patients. For those aged from 30 to 50 years, ventricular tachycardia should be controlled by antiarrhythmic agents for the prevention of SD. In patients with DCM, 24% of all cardiac deaths were attributed to SD. Although no variables reliably predicted SD, it was of note that only one patient out of 26 with SV1 + RV5 greater than or equal to 35 mm died suddenly. Whereas ventricular arrhythmias are known to be a contributing cause for SD, the prognostic significance of ventricular tachycardia on electrocardiographic monitoring in predicting SD has not yet been established. In addition, antiarrhythmic agents often precipitate hemodynamic deterioration. It therefore appears that use of antiarrhythmic agents is not a therapy of first choice and that primary treatment should be focused upon improvement in ventricular function in order to prevent SD in patients with DCM.
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PMID:Sudden death in hypertrophic and dilated cardiomyopathy. 263 25


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