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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty four cases with myocardial rupture among 259 patients with autopsy after death due to myocardial infarction, were compared with patients with acute myocardial infarction and death secondary to other causes. Myocardial rupture occured during the first 72 hours in 58% of the patients and all cases within the first five days. Two thirds of the patients were males and 46% were 70 years of age. There were 24 myocardial ruptures (9.5%). Previous history of arterial hypertension and un-remittent anginal pain were predisposing factors for rupture (p=0.05). Other previously reported bad prognostic factors such as persistent hipertension after acute infarction, severe exercise before infarction and history of Diabetes Mellitus were not statistically significant in this study. Ruptured myocardium was not influenced by a previous history of myocardial infarction, hospitalization delay in the C.C.U., administration of anticoagulants, digitalis or pressor amines. There was no significant difference among the groups compared in enzyme curves or magnitude of leucocytosis. Electromechanic dissociation, sinus bradycardia, nodal rhythm followed by idioventricular rhythm and asystole, were observed following myocardial rupture.
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PMID:[Rupture of the free wall of the heart as cause of death in acute myocardial infarct]. 66 44

The rupture of the heart wall is a severe complication of the acute myocardial infarction. We found it in 3.5% of the deceased patients with an acute myocardial infarction. The average age of these patients was 71 years. 75% of the patients died during the first five days after the event of the myocardial infarction. Apart from elderly patients with myocardial infarction such ones with a transmural myocardial infarction in the region of the left ventricle, an enlargement of the heart and signs of an insufficiency of the left heart, with a hypertension and diabetes mellitus seemed to be endangered. These patients need the most exact control and observation and in case of suspicion (symptomatology of angina pectoris which is continuing to exist) of a developing rupture of the heart wall and aimed diagnostics (echocardiography) and therapy must be begun immediately.
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PMID:[Heart wall rupture as a grave complication of acute myocardial infarct]. 223 50

In all autopsied cases from January 1980 to June 1988 (56-102 years old, 243 men and 307 women), cardiac rupture death was observed in 14 cases out of 68 deaths of acute myocardial infarction in our hospital. Cardiac rupture occurred in 2, 4, 3, and 5 cases in their 60's, 70's, 80's, and 90' respectively, and 4 in men and 10 in women. Complaints of chest pain were present in 4 cases. Cerebrovascular disease was present in 9 cases and hypertension in 7. In 9 cases, the thickness of the ruptured wall was over 14 mm. The location of the ruptured lesion was the anterior wall in 4 cases, anteroseptal in 3, anterolateral in 1, lateral in 1, posterior in 1, and apical in 1. In conclusion, the incidence of cardiac rupture was higher in female than in males, and in silent myocardial infarction than in painful one. The location of rupture was frequently in the anterior or lateral wall. Aging and hypertension would not be a worsening factor in the pathogenesis of cardiac rupture in myocardial infarction, but cerebrovascular disease might be a risk factor in respect to masking occurrence of myocardial infarction.
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PMID:[A clinicopathological analysis of cardiac rupture following acute myocardial infarction in elderly patients]. 263 25

Cardiac rupture occurs in 10 per cent of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Twenty randomly selected patients with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the two groups (5.7 +/- 5.8 days for patients with rupture versus 4.2 +/- 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the two groups, with 55 per cent of the patients with cardiac rupture having single-vessel disease and 70 per cent of the patients without cardiac rupture having disease in three vessels. Additionally, the incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in ten high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P less than 0.01) greater in hearts associated with cardiac rupture (29.5 +/- 4 per cent) than in control hearts (11.7 +/- 3.1 per cent). It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.
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PMID:Association of eosinophils with cardiac rupture. 399 34

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

A retrospective study of autopsies was performed on patients who died of ischaemic heart disease (IHD) in the industrialised Ruhr valley of West Germany. Groups were classified on the basis of the presence or absence of cardiac scar tissue, acute myocardial infarction and cardiac rupture. Severe coronary atherosclerosis was not a constant finding in IHD, and ranged from 57% of acute coronary insufficiency cases in women to 86% of recurrent infarction cases in men. During the period 1970 to 1979 recurrent infarction decreased in frequency, whilst hearts with scar tissue in the absence of fresh infarction (chronic progressive coronary insufficiency) became increasingly common. These two groups accounted for 72% of IHD deaths and were more common in men than in women. However, the incidence of first-time acute myocardial infarction and acute coronary insufficiency was higher in women than in men. The frequency of clinically known diabetes mellitus and/or hypertension was higher in women with IHD than in controls. Systemic hypertension was not commoner in cardiac rupture cases than in other cases of acute myocardial infarction. Cardiac rupture increased markedly in the latter half of the last decade so that since 1974 20% of all acute myocardial infarcts showed cardiac rupture. The incidence of first-time infarction as well as anterior infarction was significantly higher in cases of cardiac rupture than in acute infarction without rupture. The incidence of recent coronary thrombosis was low in recurrent myocardial infarction (23%), higher in first-time infarction (39%) and highest in cardiac rupture (59%). In men, this finding was significantly higher in acute infarction with rupture than in acute infarction without rupture (p less than 0.001). The view of coronary thrombosis as a secondary phenomenon in acute myocardial infarction is supported.
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PMID:Myocardial infarction, cardiac rupture, and coronary insufficiency in the industrialised Ruhr valley. An autopsy study. 685 29

Out of 762 patients with acute myocardial infarction .184 (24.15%) were with a lethal end. The basic causes of death were cardiac weakness (28.26%), rhythm and conduction disturbances (25.0%), cardiac rupture (24.45%), cardiogenic shock (16.30%) and thromboembolia (5.91%). Cardiac weakness was established as a death cause to be associated with the age between 60 and 70, male patients, anterior site of infarction, healed heart infarction and considerable lesion of the coronary arteries. Rhythm death is characteristic for young age, posterior site of infarction, lesion of septum in patients with diabetes mellitus. Cardiac rupture was a frequent cause for death among females, arterial hypertension, anterior apical site of infarction and massive, transmural infarction with insignificant lesions of the coronary arteries. The cardiogenic shock was the lethal cause in patients with a past history of infarction, severe alterations in the coronary arteries, posterior site of the infarction, with diabetes mellitus and female patients.
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PMID:[Factors affecting the cause of death in the acute stage of myocardial infarct]. 741 58

In patients with acute myocardial infarction (AMI) since a decrease of deaths due to arrhythmia control and pump failure, rupture of the left ventricle free wall (RPL) has gained increasing importance as a cause of death. Of 4987 patients hospitalised for AMI from January 1969 to December 1993, RPL occurred in 121 patients (2.4%) and 17.6% of total deaths from AMI are the result of this complication. RPL was found more often in women > 75 years old, with a history of hypertension and sustaining a first coronary event. Cardiac rupture occurred after transmural myocardial necrosis, usually (60%) following an anterior AMI. RPL was an early phenomenon (in 40% it occurred within the first 24 hours and in more than 80% within 5 days from symptoms onset). Although RPL is widely considered catastrophic and unexpected, in the greater number of patients it is possible to recognise symptomatic markers (pain, emesis and agitation) indicative of impending rupture. A prompt diagnosis and the consideration that rupture is usually a stuttering process must point out an aggressive approach, which can allow a surgical treatment of RPL with a likely prognosis.
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PMID:[Identification of patients at risk of post-infarction heart rupture. Clinical and therapeutic characteristics of 121 consecutive cases and review of the literature]. 764 85

Myocardial rupture is a lethal complication of acute myocardial infarction. The concurrence of myocardial infarction and hypertension is known to predispose to cardiac rupture. Therefore, it is likely that postinfarction cardiac rupture in the presence of severe aortic stenosis will lead to a rapidly fatal outcome due to the associated left ventricular hypertension. We report survival in a patient with postinfarction left ventricular free wall rupture discovered at operation for severe aortic valve stenosis.
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PMID:Survival after postinfarction cardiac rupture in severe aortic valve stenosis. 817 76

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.
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PMID:[A 62-year-old man with an acute onset of consciousness disturbances]. 945 48


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