Postinfarction Cardiac Rupture Research Articles

Postinfarction cardiac rupture despite immediate reperfusion therapy in a patient with severe aortic valve stenosis

A 74-year-old woman with severe aortic valve stenosis (AS) was admitted to our hospital because of dyspnea on exertion. On day 2, she developed acute anterior wall myocardial infarction (MI) with ST elevation. Tissue plasminogen activator (tPA) was administered 10 min after the onset of chest pain, and emergency percutaneous coronary intervention was performed to induce coronary reperfusion after another 50 min. Five hours after MI onset, however, she suddenly went into electromechanical dissociation and died from cardiac rupture. This is the first case report of postinfarct cardiac rupture with severe AS occurring in spite of instituting immediate reperfusion therapy. High intraventricular pressure may be a critical risk factor for cardiac rupture in patients with AS complicated with acute MI. Further studies are required to clarify the risk and benefit of tPA administration before percutaneous coronary intervention and the necessity of the emergency correction of AS to prevent cardiac rupture.

Sutureless Repair With TachoComb Sheets for Oozing Type Postinfarction Cardiac Rupture

Left ventricular free-wall rupture is a well recognized complication of myocardial infarction and a frequent cause of death. The appropriate surgical management varies significantly depending on the condition of the tear and the presence of concomitant lesions. We present a case of oozing type postinfarction cardiac rupture that was treated successfully by a sutureless patch technique using a fibrin tissue-adhesive collagen fleece (TachoComb [Torii Pharmaceutical, Tokyo, Japan]). This represents a quick, effective, and safe option for dealing with oozing type myocardial rupture due to myocardial infarction.

Post-infarction cardiac rupture: surgical treatment.

Rupture of ventricular free wall (VFWR) may complicate acute myocardial infarction and accounts for high mortality. Surgical repair is the only therapeutic option. A review of our surgical experience is presented. Seventeen patients (11 men, mean age 68 years) underwent surgery for VFWR. Patch covering technique was used in 13 patients, infarctectomy with patch reconstruction in three patients, direct suture without patch in one patient. Coronary artery bypass grafting was performed in eleven patients. Hospital mortality was 17.6% (three patients). Three patients died of cancer during the follow-up. The remaining 11 patients are in good condition after a mean follow-up of 45.8 months (range 7.5-84.2). Postinfarction rupture of ventricular free wall treated surgically gives excellent long-term results. Our first choice for repair is the covering technique with a large pericardial patch anchored with biological glue and epicardial sutures.

Increased collagen content reduces the risk of post-infarct cardiac rupture in mice that overexpress β2-adrenergic, receptors in the heart

Increased collagen content reduces the risk of post-infarct cardiac rupture in mice that overexpress β2-adrenergic, receptors in the heart

Morphopathology of myocardial infarction in hypertension. a postmortem study

Although a large series of studies identified hypertension as a major coronary risk factor for all the types of myocardial ischemic disease, only a few reports related the morphology of acute myocardial infarction (AMI) to hypertension. Remodeling from cardiac hypertrophy due to hypertension would often seem to lack in AMI hearts. The purpose of this study was to assess retrospectively the relationship between pre-existing hypertension and morphopathology of AMI. We re-examined 168 (56.7%) autopsy cases out of 296 affected by AMI. 108 (64%) were males and 60 (36%) females with a mean age of 64.3 ± 18 years. 27/168 AMI pts (16%) had hypertension (systolic blood pressure from 180 mmHg to 220 mmHg, and diastolic blood pressure from 90 mmHg to 115 mmHg). Anatomically, infarction was anterior 86 times (51%)-13 cases (15%) with hypertension-, inferior 49 times (29%)-9 cases (18%) with hypertension-, and anterior+inferior 33 times (20%)-5 cases (15%) with hypertension-. 10 hypertensive hearts (37%) showed postinfarction cardiac rupture (PCR) with cardiac hypertrophy (mean heart weight: 627 ± 188 gm, wall thickness 25 ± 3 mm versus respectively 400 ± 75 gm, and 14 ± 2 mm for non-hypertensive hearts and hypertensive hearts without PCR, P < 0.01). No change in pathologic patterns of AMI was seen. Multiple irregular narrowings less than 90% affected coronary tree of hypertensive hearts compared with hearts without hypertension (P < 0.01). No difference in occlusive thrombi. In conclusion, hypertension influenced morphopathology of AMI by a greater number of stenoses in the coronary tree and a major incidence of PCR accompanied by cardiac hypertrophy.

Pericardial hood repair of cardiac rupture secondary to extended myocardial infarction

A surgical technique for simple and safe repair of oozing-type postinfarction cardiac rupture secondary to extended myocardial infarction is described. A hood-shaped pericardium was glued with gelatin-resorcinol and formaldehyde glue to cover the extended oozing infarcted myocardium. This technique was used on 3 elderly patients with good results.

Role of collateral circulation of the infarcted area in patients with postinfarction cardiac rupture

Role of collateral circulation of the infarcted area in patients with postinfarction cardiac rupture

Double Postinfarction Cardiac Rupture of Left Ventricular Free Wall and Papillary Muscle Documented by Transthoracic Echocardiography

A 70-year-old man presented with a posteroinferolateral acute myocardial infarction complicated by rupture of the left ventricular inferior wall and partial rupture of the posteromedial papillary muscle. Transthoracic echocardiography documented both of these complications and led to prompt and successful surgical repair. (J Am Soc Echocardiogr 1998;11:1084-6.)

New strategy for successful repairment of post infarction cardiac rupture

Reperfusion therapy for acute myocardial infarction (AMI) has reduced early mortality, however the incidence of cardiac rupture following AMI has not significantly decreased. Cardiac rupture is a catastrophic complications and there are few reports of patients who have successfully recovered. The percutaneous cardiopulmonary support system (PCPS) is useful in maintaining circulation during circulatory collapse. Surgical interventions using PCPS were performed in eleven patients with cardiac rupture. Attempts at surgical repair were possible in six patients when PCPS was used as the circulatory assist deveice. On the other hand, when PCPS was used as a circulatory assistance device, but none survived. PCPS was used in five patients as both a circulatory assistance device and for surgical support at low temperature (20°C). Two of these five patients survived and were uneventfully discharged. This new strategy of using hypothermic percutaneous cardiopulmonary support bypass should prove to be useful for successful repair of post-infarction rupture.

Clinicopathological characterization of cardiac free wall rupture in patients with acute myocardial infarction: difference between early and late phase rupture

Differences in morphological characteristics have been described in early phase and late phase post-infarction cardiac rupture. In this study, the clinicopathological characteristics of early and late phase rupture have been clarified by reviewing the clinical records of 1450 consecutive patients with acute myocardial infarction (AMI). Rupture of the left ventricular free wall (blow-out type) developed in 27 of the 1450 patients, and these patients were divided into two groups on the basis of the rupture time: early phase (< 72 h) and late phase (> 4 days). Only one patient had a history of prior infarction. Early phase rupture was characterized by an abrupt slit-like tear in the infarcted myocardium, a preference for anterior infarction sites, no prior myocardial infarction, and no difference in incidence in conventional and reperfusion therapy, while late phase rupture was characterized by the presence of infarct expansion, no preferential infarct site and a very low incidence in patients with successful reperfusion. Hence, early and late phase cardiac rupture differ in their pathogenesis, and thus the approach to the prevention and prediction of early and late phase cardiac rupture should be different.

Are We Able to Prevent Death Due to Postinfarction Cardiac Rupture by Early Diagnosis and Surgical Treatment?

Death from postinfarction cardiac rupture (PCR) may occur in two ways. There are patients who die suddenly without symptoms or with symptoms of less than an hour's duration (sudden cardiac death), whereas other patients die several hours after the onset of the rupture. Ninety-six patients who died from AMI and underwent autopsy have been studied. Sixteen patients displayed a rupture of the free wall of the left ventricle at the site of infarction, cardiac hypertrophy and severe coronary alterations. Six of these patients were included among patients who died suddenly. The other 10 showed signs before death that occurred from 240 to 660 min after their appearance. Signs of impending rupture were appearance or increase of chest pain that was not improved by opiates, preterminal sinus rhythm with an unchanged ST-segment and echocardiographic infarct expansion or pericardial effusion. We propose that the emergence of these signs during AMI suggests an impending rupture. Early surgical intervention is essential to save those patients who survive several hours after the initial signs of PCR.

A case of postinfarction cardiac rupture following to PTCR

A case of postinfarction cardiac rupture following to PTCR

Surgical repair of acute postinfarction cardiac rupture

Acute myocardial infarction is complicated by cardiac rupture in 4% to 24% of all infarction deaths, and approximately 10% of hospital infarction deaths. There are no reliable indices to determine which patients run an increased risk of cardiac rupture. This report describes the surgical treatment and outcome of a patient who sustained a rupture of the left ventricular free wall, nine days after extensive anterior myocardial infarction.

POSTINFARCTION CARDIAC RUPTURE

Eight fatalities due to cardiac rupture, of 40 consecutively autopsied myocardial infarctions, were clinicopathologically examined. Total duration of infarctions in 8 cases ranged from 9 hours to 14 days. The longer the period, the more the infarction extended, and aneurysmal dilatation of infarcted wall and tissue weakness were striking. The weakness was caused by the lack of replacement of necrotic muscle fibers by granulation, and was related to aneurysmal structure per se and also to its paradoxical pulsations. Postinfarction cardiac rupture occurring in relatively later phase was considered to be mainly due to weakness of infarcted wall, with less influence factors of mechanical stress such as physical exertion, hypertension, or intracardiac pressure. In the case where cardiac rupture took place in a relatively early stage of the episodes, infarction covered only a small range and aneurysmal change of the ventricle was slight, for which dynamic factors, represented by the degree of a localized strain elicited by myocardial contraction of non-infarcted site, seemed to play a significant role.

Coronary artery narrowing without irreversible myocardial damage or development of collaterals. Assessment of "critical" stenosis in a human model.

Postinfarction cardiac rupture is the result of thrombotic occlusion of a functional end artery with no previous myocardial damage in the perfusion area of the occluded artery. The pre-existing atherosclerotic stenosis at the site of thrombosis is thus"non-critical" in relation to development of collateral vessels and/or irreversible myocardial damage. Eleven cases of postinfarction cardiac rupture were studied by microscopy of cross-sections of the thrombosed segments. At the site of the thrombosis, pre-existing atherosclerosis had narrowed the lumen to 11% or less of its normal cross-sectional area. Maximal pre-existing narrowing of the proximal left anterior descending artery was found in a case with 97% stenosis (histologically measured cross-sectional area reduction) and an estimated residual lumen of 0.71 mm2. The prestenotic luminal area which is usually considered angiographically as "normal" was in all cases shown histologically to be severely narrowed by a diffuse intimal thickening. It is concluded that organic coronary stenosis must be far greater than 75% to be responsible for the development of collateral vessels and/or irreversible myocardial damage.

Postinfarction Cardiac Rupture: Surgical Success and Review of the Literature

Cardiac rupture following myocardial infarction has been reported as the cause of 4 to 24% of all infarction deaths. The rupture may occur from a few hours to several days after the myocardial infarction and is not a true “blowout” but rather a necrotic hemorrhagic area in the center of the infarction that extravasates blood and leads to pericardial tamponade. The most common findings when rupture occurs are renewed chest pain, bradycardia, and shock. Two patients with postinfarction myocardial rupture who were operated on successfully are reported. With prompt diagnosis and treatment, more of these patients would survive long enough to undergo operation. With cardiopulmonary bypass the repair of these ruptures is not difficult.

Cardiac rupture during myocardial infarction. A review of 44 cases.

Forty-four cases of myocardial infarction with cardiac rupture, 88 cases of unruptured myocardial infarction, and 88 cases without myocardial infarction were studied retrospectively. The incidence of cardiac rupture in cases with acute myocardial infarction alone was 5.5% while in hearts having both healed and acute myocardial infarction the incidence was 2.3%. One instance of cardiac rupture was encountered in a heart having only a healed myocardial infarction with subsequent aneurysmal dilation of the healed infarct. Although females represented only 37% of the population having acute myocardial infarction in this institution, they accounted for 55% of the cases of cardiac rupture. On the average the hearts which ruptured following myocardial infarction were lighter and thinner than in the control group of patients having infarction without rupture. Among the clinical correlates possibly associated with postinfarction rupture the most significant finding in the present study is the presence of postinfarction hypertension. In the group of cases with cardiac rupture this was present in 40% while in the control group not having suffered cardiac rupture the comparable figure was 14%. A history of diabetes was found in 18% of the cases of myocardial infarction not having suffered cardiac rupture. A similar history was found in only 9% of the cases having a postinfarction cardiac rupture. This latter incidence is identical with the frequency of diabetes mellitus in the general autopsy population. There is a suggestion that early and severe atherosclerosis may cause earlier heart disease and when infarction occurs provide some protection against rupture. Of interest among the 44 cases of cardiac rupture, none of the patients had cirrhosis, in striking contrast to the 11% incidence of this condition in our general autopsy population.