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Query: UMLS:C0018801 (heart failure)
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A retrospective study of 100 case notes of patients who died from a recent myocardial infarction (less than one month before death) has established the causes of death: cardiac failure (52), rupture of the heart (40), major pulmonary emboli (3), primary irreversible ventricular fibrillation (2), unexplained death (3). Study of the extent of the necrosis by the technique of segmentation of the ventricular mass has allowed us to clarify the correlation between the "index of extent" ("i"), an the clinico-pathological findings. It has been noted in particular that those infarctions complicated by cardiogenic shock and/or by bilateral bundle branch block were those with the highest value of index of extent (i = 8.91, i = 9.40); also that cardiac failure and ventricular tachycardia were found in the extensive infarctions (i = 7,33, i = 9.52); also that rupture of the outer wall and pulmonary thromboses complicated infarctions of very small extent (i = 4,80, i = 5,67). It would not seem possible to reduce the hospital mortality of infarctions significantly, since it is essentially linked with circulatory failure caused by extensive necrosis, and with ruptures of the heart which are unpredictable and untreatable.
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PMID:[Cause of death in recent myocardial infarct. Correlation between extent of necrosis and clinical, electrocardiographic and anatomical findings]. 41 79

In a series of 51 clinico-pathological examinations on patients who died during the first 15 days after the onset of clinical symptoms of their first and only transmural myocardial infarction (anterior: 29 cases; posterior: 22 cases) the causes of death were divided into: heart failure -- 26 cases (53 p. 100); rupture of the heart -- 22 cases (43 p. 100); disorders of ventricular rhythm -- 2 cases (4 p. 100). The anatomical basis of fatal cardiac failure is twofold: either a very extensive area of necrosed muscle, of poor quality of the mass of muscle not involved in the infarction. In the anterior infarctions (16 cases, representing 55 p. 100 of deaths in this group) the first factor was foremost, the mean extent of necrosed muscle constituting 42 p. 100 of the total left and septal ventricular mass; stenotic coronary lesions, which were commonly found on the anterior descending artery, were confined to this artery alone in 10 cases 62 (p. 100). In posterior infarctions (11 cases, representing 50 p. 100 of deaths in this group), the mass of muscle destroyed was less (mean 36 p. 100), but the stenotic coronary lesions were diffuse, involving the three main trunks in 9 cases, which also explains the poor quality of the muscle not involved by necrosis. Thus there is a clear difference between anterior and posterior infarctions followed by deaths from cardiac failure: in the first group, the remaining muscular mass is quantitatively insufficient to maintain the haemodynamics, while in the second it is qualitatively insufficient, because of poor blood supply, to maintain an adequate cardiac output.
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PMID:[Fatal cardiac insufficiency in the course of an initial acute myocardial infarct. Anatomical-clinical data]. 41 80

Clinical and autopsy study of 100 cases of patients dying during the first 3 weeks of hospitalisation for myocardial infarction revealed the following causes of death: cardiac failure in 59 cases (including 40 of cardiogenic shock), rupture of the heart in 29 cases (24 of rupture of the ventricular wall, 4 of the septum and 1 of a mitral papillary muscle). 4 ventricular arrhythmias and 6 haemorrhagic or embolic complications. In 2 cases, the cause of death could not be accurately determined. In cardiogenic shock, death usually occurred early. It was later in cases of refractory left ventricular failure. Conduction disturbances were much commoner in cases of myocardial infarction complicated by fatal cardiac failure (57.6%) than in the presence of any other complication (17.1%) (p less than 0.001). The responsible infarction was often extensive and recurrent. Rupture of the heart invariably occurred during the first three days of an infarction often initial (p less than 0.001), anterior (apart from septal rupture) and small in size (p less than 0.01). Other complications play only a secondary role in mortality at the present time, in particular arrhythmias, the gravity of which has greatly decreased since the reduction of delays before hospitalisation and improvements in anti-arrhythmic therapy.
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PMID:[Clinicopathological study of the causes of mortality during the acute phase of myocardial infarction (author's transl)]. 74 57

Post-infarction free-wall, papillary muscle and septal myocardium rupture yields a lowering mortality, not only due to the improved surgical technique but also to a more careful selection of surgical candidates. The value of pericardial decompression in cases of free-wall rupture is discussed. Echocardiographic evidence of blood in the pericardium after a myocardial infarction is not a direct indication for a diagnostic sampling, decompression or surgery. Pericardiocentesis is not a risk-free procedure and should be limited to patients with life-threatening acute tamponade. Clinical results of 34 patients operated upon for myocardial rupture, regardless of adopted technique or timing of surgery, confirm that the decision about a patient's operability should follow a careful evaluation of the following risk factors in this order: infarct size, age, cardiogenic shock, multiorgan failure, rupture site, cardiac failure and associated diseases.
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PMID:[Acute surgically-treated complications of myocardial infarct. Clinical experience and discussion of surgical indications]. 162 80

Doppler echocardiography, providing objective data on heart anatomy and cardiac function, is a diagnostic method of unquestionable value in the acute phase of myocardial infarction. In what concerns myocardial infarction complications; echocardiography permits: a) evaluation of ventricular function, by quantifying heart failure and establishing the diagnosis of ventricular aneurysm; b) it is the most reliable method in the diagnosis of thrombi, and c) it constitutes a fundamental diagnostic tool in mechanical complications: rupture of the heart structures and evaluation of valvular competence. a) Evaluation of ventricular function. The analysis of ventricular dimensions and segmentary wall motion abnormalities permits the quantification of the infarct size and its repercussion upon the cardiac function. Otherwise, left ventricular proto and end diastolic filling rates give an idea about ventricular diastolic function alterations. b) Ventricular thrombi. The incidence of ventricular thrombi in AMI is variable, depending on the site of infarction and the number of segments with wall motion abnormalities. By echocardiography it has been demonstrated that 40% of the anterior transmural myocardial infarctions and 10% of the inferior ones disclosed thrombi, although the incidence of systemic embolism is scarce and similar on both anterior and inferior infarctions: nearly 2% during the first month after infarction. The criteria that identify the embolic risk include: thrombus size over 2 x 2 x 2 cm, pediculated and mobile thrombi. On the other hand, right intraventricular thrombi incidence is rare nearly 5% of right ventricular infarctions and post-infarction pulmonary embolism is probably more related to peripheral venous thrombus than to an intraventricular one. c) Mechanical complications. Echocardiography enables the direct diagnosis of interventricular septum and papillary muscles rupture in about 80% of the cases and although ordinary does not provide direct data on free ventricular wall rupture, the detection of pericardial effusion with high density echoes, together with finding of free right ventricular and atrial wall collapse, gives 80% of sensibility and over 90% of specificity in the diagnosis of free ventricular wall rupture. Finally, Doppler echocardiography permits the diagnosis and quantification of mitral and tricuspid regurgitation secondary to a rupture of even a simple disfunction of the atrioventricular subvalvular apparatus.
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PMID:[Usefulness of Doppler echocardiography in the diagnosis of complications in the acute phase of myocardial infarct]. 220 45

The occurrence of myocardial rupture was studied in a well defined unselected population of patients with acute myocardial infarction, and the group of patients who died of rupture of the heart were compared with two control groups. Of a total of 3960 patients, 1746 (44%) fulfilled the diagnostic criteria for acute myocardial infarction. Rupture was defined solely on the basis of the presence of a pathological passage through part of the myocardium, either the free wall of the left ventricle or the septum, found at necropsy or during operation. Two controls were selected for each patient and matched for age and sex, one (control group A) with acute myocardial infarction having died in hospital but not of rupture (non-rupture cardiac death) and one (control group B) with acute myocardial infarction having survived the hospital stay. Necropsy was performed in 75% of all fatal cases with acute myocardial infarction. The total hospital mortality was 19%, the highest mortality being among women over 70 years (29%). Ruptures (n = 56) were found in 17% of the hospital deaths, or 3.2% of all cases of acute myocardial infarction. Women aged less than 70 had the highest incidence of rupture, 42% of deaths being due to rupture. The mean age for patients with rupture and controls was 70.5 years. The median time after admission to death was approximately 50 hours for patients and control group A. Thirty per cent of the patients with rupture occurred within 24 hours of the initial symptoms occurring. Angina and previous acute myocardial infarction were more common among control group A. Patients with rupture and control group B were mostly relatively free of previous cardiovascular or other diseases (chronic angina pectoris ( > 2 months) and previous myocardial infarction). Sustained hypertension during admission to the coronary care unit was more common in patients than in control group A. Hypotension and shock were more common among control group A. Most (79%) of the patients who subsequently ruptured did not receive any corticosteroids at all during the hospital stay. Severe heart failure and antiarrhythmic treatment were more uncommon among patients than among control group A. Patients with rupture received analgesics approximately three times a day throughout their stay. Control group B received analgesics mostly during the first 24 hours. Thus female patients, patients with first infarcts, and patients with sustained chest pain should be investigated for the possibility of rupture. As many as one third (32%) of ruptures may be subacute, and therefore time is available for diagnosis and surgery.
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PMID:Rupture of the myocardium. Occurrence and risk factors. 401 10

Acute rupture of the left ventricular free wall was suspected in a 53 year old hypertensive patient at the 12th hour of primary antero-septo-apical myocardial infarction. He developed acute tamponade with severe cardiogenic shock during his transfer to hospital. Cardiac compression due to hemopericardium was confirmed by M mode echocardiography (pericardial effusion), right heart catheterisation (adiastole and low cardiac output) and pericardial puncture during which several ccs of blood were aspirated leading to a slight improvement in the patient's condition. At operation under cardiopulmonary bypass 2,5 hours after hospital admission, the surgeon found a hemopericardium related to fissuration of an acute apical infarct which was sutured on a Teflon support. The initial postoperative course was complicated by unexplained gastro-intestinal hemorrhage, transient functional renal failure, cardiac failure and mediastinitis, but the final outcome was successful with a follow-up of 24 months. This appears to be the 9th reported case of long-term survival after surgical repair of rupture of the heart in the acute phase of myocardial infarction.
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PMID:[Acute rupture of the left ventricle 12 hours after an anteroseptal myocardial infarct. Successful surgical repair]. 640 36

Cardiac rupture is a fatal complication of acute myocardial infarction lacking treatment. Here, acute myocardial infarction resulted in rupture in wild-type mice and in mice lacking tissue-type plasminogen activator, urokinase receptor, matrix metalloproteinase stromelysin-1 or metalloelastase. Instead, deficiency of urokinase-type plasminogen activator (u-PA-/-) completely protected against rupture, whereas lack of gelatinase-B partially protected against rupture. However, u-PA-/- mice showed impaired scar formation and infarct revascularization, even after treatment with vascular endothelial growth factor, and died of cardiac failure due to depressed contractility, arrhythmias and ischemia. Temporary administration of PA inhibitor-1 or the matrix metalloproteinase-inhibitor TIMP-1 completely protected wild-type mice against rupture but did not abort infarct healing, thus constituting a new approach to prevent cardiac rupture after acute myocardial infarction.
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PMID:Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. 1050 7

Free wall rupture of the heart is the most common cause of death following pump failure. The incidence of death is 10-16% of all deaths because of acute myocardial infarction (AMI). In respect of time between the onset of AMI to Cardiac Rupture (CR), early (80%) and late CR are distinguished. Other clinical classification distinguishes acute and subacute CR. CR is considered subacute if the time between the onset of typical symptoms of CR and irreversible shock is longer as 30 min. There are three problems to solve: 1) selection of patient particularly threatened with CR, 2) defining the prodroms of CR and early diagnosis, 3) advancing the methods of surgical treatment. CR occurs more often in women, hypertensive patients and patient > 60 years old sustaining the first infarction. Thrombolytic agents diminish overall mortality in AMI, but do not influence frequency of CR. There are three mechanisms of CR incidence: 1) blood effusion into the ischemic zone resulting in the loss of tissue strength, 2) influence of thrombolytic therapy on degradation and inhibition collagen synthesis, 3) absorption of collagen by lymphocyte infiltration in infarction zone. Cardiac insufficiency with cardiogenic shock and rapid increase of pericardial effusion in echo examination and electro-mechanical discordance are considered to be clinical signs of CR and tamponade. CRP is an independent marker of subacute CR. Surgical treatment is possible only in case of subacute CR. Pericardiocentesis and bloodletting could temporary diminish cardiac tamponade and allow transfer to the operating room.
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PMID:[Cardiac rupture in acute myocardial infarction]. 1071 Sep 44

The morphological characteristics of post-infarction ventricular remodeling were determined by comparison of infarct location and histological changes of noninfarcted myocardium at autopsy. A total of 94 cases of first acute myocardial infarction with clinical courses of 0 to 37 days were studied. Hearts were sliced on the short axis at the level of 1/3 of the distance from the atrioventricular ring to the apex. Wall thicknesses of the infarcted and noninfarcted areas, and the endocardial and epicardial perimeter lengths of the left ventricle were measured. Myocyte diameter and number of myocytes in the noninfarcted area were measured. Infarcts were classified into 3 groups based on infarct location (51 anterior, 22 posterior, and 21 nontransmural circumferential) and each group was further divided according to the clinical course of less than 72 hours or longer. Fifty two patients died within 72 hours. Cardiac rupture was the most common cause of death in the anterior group. Patients in the posterior group chiefly died due to cardiogenic shock and in the circumferential group chiefly died to pump failure. According to the number of stenosed coronary arteries, cardiac rupture was the most common cause of death in single-vessel disease in both anterior and posterior groups (62.1% and 55.6%, respectively). In double-vessel disease, the most common cause of death in the anterior group was still cardiac rupture (50.0%). On the other hand, 50.0% of the posterior group died of cardiogenic shock in double-vessel disease. Patients with triple-vessel disease mainly died due to heart failure in all groups. Wall thickness of the infarcted myocardium was decreased in the anterior group after 72 hours (11.8 +/- 3.5 vs 7.8 +/- 2.5 mm). Endocardial perimeter length was increased in the anterior and circumferential groups (83.6 +/- 25.6 vs 116.3 +/- 29.5 mm, 75.2 +/- 12.0 vs 117.6 +/- 3.1 mm, respectively). Endocardial/epicardial perimeter length ratio increased with longer clinical course in the anterior group. No specific change in wall thickness or perimeter length was found in the posterior group. Noninfarcted wall thickness was preserved in both the anterior and posterior groups. Myocyte diameter and number of myocytes in the noninfarcted area showed no significant difference after 72 hours. The nature of ventricular remodeling differs with infarct location. Ventricular dilation occurred during the clinical course in the anterior group. The transmural and adjacent areas are more important than the remote noninfarcted area in post-infarction remodeling within this period.
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PMID:[Clinicopathological study of left ventricular remodeling after first acute myocardial infarction]. 1083 76


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