Spontaneous Rupture of the Heart

Levene, Arnold

doi:10.1136/hrt.22.5.660

Cited by 12 publications

(3 citation statements)

References 20 publications

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“…The early phase of cardiac remodeling involves expansion of the infarct zone, resultant from degradation of the intermyocyte collagen and activation of matrix metalloproteinases (MMPs) (128). Protein breaks, coagulative necrosis, influx of inflammatory cells, even a severe consequence of a possible rupture of the free wall, may occur usually a few days post-MI (75,81).…”

Section: Structure/pathologymentioning

confidence: 99%

Innate immune response in the pathogenesis of heart failure in survivors of myocardial infarction

Zimmer

Bagchi

Vinayak

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Among the different cardiovascular disease complications, atherosclerosis-induced myocardial infarction (MI) is the major contributor of heart failure (HF) and loss of life. This review presents short- and long-term features of post-MI in human hearts and animal models. It is known that the heart does not regenerate, and thus loss of cardiac cells after an MI event is permanent. In survivors of a heart attack, multiple neurohumoral adjustments as well as simultaneous remodeling in both infarcted and noninfarcted regions of the heart help sustain pump function post-MI. In the early phase, migration of inflammatory cells to the infarcted area helps repair and remove the cell debris, while apoptosis results in the elimination of damaged cardiomyocytes, and there is an increase in the antioxidant response to protect the survived myocardium against oxidative stress (OS) injury. However, in the late phase, it appears that there is a relative increase in OS and activation of the innate inflammatory response in cardiomyocytes without any obvious inflammatory cells. In this late stage in survivors of MI, a progressive slow activation of these processes leads to apoptosis, fibrosis, cardiac dysfunction, and HF. Thus, this second phase of an increase in OS, innate inflammatory response, and apoptosis results in wall thinning, dilatation, and consequently HF. It is important to note that this inflammatory response appears to be innate to cardiomyocytes. Blunting of this innate immune cardiomyocyte response may offer new hope for the management of HF.

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Section: Structure/pathologymentioning

confidence: 99%

Innate immune response in the pathogenesis of heart failure in survivors of myocardial infarction

Zimmer

Bagchi

Vinayak

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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“…Subsequently, an increase in wall stress occurs which exerts a stress on the infarcted segment predisposing it to rupture (5). Another possible pathophysiologic mechanism may be related to mechanical stress placed on infarcted tissue by the forcible contraction of the surrounding normal tissue (5,35). Both mechanisms can be exaggerated by the presence of persistent or postinfarct hypertension.…”

Section: Pathophysiologymentioning

confidence: 99%

Ventricular Free Wall Rupture in Acute Myocardial Infarction

Khalil

Heller

Boctor

et al. 2001

J Cardiovasc Pharmacol Ther

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Despite a progressive reduction in acute myocardial infarction mortality over the years, death related to ventricular free wall rupture has not changed. This is mostly related to the catastrophic presentation and death within minutes in the majority of these patients. Once rupture is suspected, bedside echocardiography should be performed immediately, followed by pericardiocentesis and repair of the rupture site as quickly as possible. Measures to prevent cardiac rupture include the administration of beta-blockers and angiotensin-converting enzyme inhibitors unless contraindications exist, and the avoidance of steroidal and nonsteroidal anti-inflammatory agents such as ibuprofen and indomethacin.

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“…circumference); one (Payne et al) was only 0 9 cm. in diameter, and Boicourt et al (1962) described the defect in their case as flap-like, but Levene (1960), in his pathological study of rupture of the heart, pointed out that myocardial tears are often oblique, and that the epicardial or right ventricular opening may be inconspicuous. These observations support the view that surgical repair is more likely to be successful when the defect is physiologically a large one; in such a case the mere fact of survival long enough for surgery to be considered indicates reasonable left ventricular function.…”

Section: Repair Of Acquired Ventricular Septal Defect After Myocardiamentioning

confidence: 99%

Successful early repair of acquired ventricular septal defect after myocardial infarction.

Honey¹,

Belcher²,

Hasan³

et al. 1967

Heart

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Successful repair of an acquired ventricular septal defect following myocardial infarction was first reported in 1962. Recently Barnard and Kennedy (1965) have reviewed 14 patients with post-infarction ventricular septal defect in whom surgical closure was attempted; 7 survived more than 6 weeks after operation. They found that those whose defects were closed 5 weeks or more after infarction survived the operation, but that those requiring emergency operation soon after infarction died. The best long-term results were obtained in those whose operations were delayed 3 months or more. However, more than 90 per cent of all patients die within a year of septal rupture, and most of these die within 2 months (Sanders, Kern, and Blount, 1956). It is clear that surgical repair should be considered in all patients who have a hemodynamically significant shunt through an acquired ventricular septal defect; ideally this should be done at least 6 and preferably 12 weeks after infarction, but, in view of the very high early mortality on medical treatment, nothing can be lost by attempting closure at an earlier stage if the patient is deteriorating.The following report concerns a patient in whom the defect was successfully repaired 27 days after infarction, and 20 days after the presumed time of septal rupture. Case ReportA man, aged 52, had left-sided chest pain, with nausea and sweating, on September 10, 1965. On September 17, he was more breathless and had a fainting episode; on this occasion his doctor heard a loud pracordial systolic murmur for the first time.On admission to the Whittington Hospital on September 20 under the care of Dr. T. St M. Norris, he was pale and sweating with a regular tachycardia and a raised venous pressure. The blood pressure was 120/100 453 mm. Hg. The heart was not clinically enlarged but a loud pansystolic murmur with thrill was loudest in the fourth left intercostal space near the sternum. There were bilateral basal rales, and a chest x-ray film showed pulmonary venous congestion with a small right pleural effusion. The electrocardiogram showed a recent posterior myocardial infarct. The diagnosis of ruptured interventricular septum was made; he improved at first on routine medical treatment, but signs of right-sided heart failure increased, and he was transferred to the London Chest Hospital on September 28 for consideration of surgical repair.At this time he was orthopnceic, and had signs of congestive cardiac failure with raised jugular venous pressure (10 cm.), enlarged tender liver, and cedema of both ankles. The pulse was rapid (110/min.) and the blood pressure 130/100 mm. Hg. The murmur and thrill were unchanged. He had several carious teeth and gross gingival infection. The chest x-rayfilm showed no cardiac enlargement (CTR 48%); there was severe pulmonary congestion with bilateral hilar and basal clouding and small pleural effusions. The electrocardiogram showed normal sinus rhythm; Q waves, slightly raised ST segments, and inverted T waves in leads II, III, aVF, V6, and V7 indicated...

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Spontaneous Rupture of the Heart

Cited by 12 publications

References 20 publications

Innate immune response in the pathogenesis of heart failure in survivors of myocardial infarction

Innate immune response in the pathogenesis of heart failure in survivors of myocardial infarction

Ventricular Free Wall Rupture in Acute Myocardial Infarction

Successful early repair of acquired ventricular septal defect after myocardial infarction.

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