Echocardiographic features of interventricular septal dissection in patients with Behçet's disease.

Involvement of the heart in Behçet's disease (BD) is rare. We retrospectively analyzed these three patients with interventricular septal (IVS) dissection in BD and discussed the echocardiographic manifestations of IVS dissections. In our patients, the echocardiographic characteristics of IVS dissection were echo-free space in the IVS basal segment or basal to middle segment, dilatation in the diastole and contraction in systole, and abnormal turbulent blood flow in the heart.

[Ventricular Septal Perforation after Inferior Myocardial Infarction].

We report a rare case of ventricular septal perforation (VSP) after inferior myocardial infarction. Surgical repair of VSP after inferior infarction is technically difficult because of its anatomical location. An 81-year-old female presented with dyspnea on the 8th day after percutaneous coronary intervention for acute inferior myocardial infarction. Echocardiography revealed a ventricular septal perforation. Urgent operation was performed. There was a VSP around the base of the ventricular septum. The myocardial infarction extended to the adjacent muscle of the mitral valve annulus. Two bovine pericardial patches were used in the left ventricular cavity. The patches were sewn on the mitral valve annulus which was the only normal tissue in the region. The 1st patch was used to close the VSP directly, and the 2nd patch was sutured to the normal myocardium to exclude the infracted area. No residual shunt flow was observed. The postoperative course was uneventful.

A collagen α2(I) mutation impairs healing after experimental myocardial infarction.

Collagen breakdown and de novo synthesis are important processes during early wound healing after myocardial infarction (MI). We tested the hypothesis that collagen I, the main constituent of the extracellular matrix, affects wound healing after MI. The osteogenesis imperfecta mouse (OIM), lacking procollagen-α2(I) expression, represents a model of the type III form of the disease in humans. Homozygous (OIM/OIM), heterozygous (OIM/WT), and wild-type (WT/WT) mice were subjected to a permanent myocardial infarction protocol or sham surgery. Baseline functional and geometrical parameters determined by echocardiography did not differ between genotypes. After MI but not after sham surgery, OIM/OIM animals exhibited significantly increased mortality, due to early ventricular rupture between day 3 and 7. Echocardiography at day 1 demonstrated increased left ventricular dilation in OIM/OIM animals. Less collagen I mRNA within the infarct area was found in OIM/OIM animals. At 2 days after MI, MMP-9 expression in the infarct border zone was higher in OIM/OIM than in WT/WT animals. Increased granulocyte infiltration into the infarct border zone occurred in OIM/OIM animals. Neither granulocyte depletion nor MMP inhibition reduced mortality in OIM/OIM animals. In this murine model, deficiency of collagen I leads to a myocardial wound-healing defect. Both structural alterations within pre-existing collagen matrix and impaired collagen de novo expression contribute to a high rate of early myocardial rupture after MI.

A severe complication after ST-segment elevation myocardial infarction (Part 2).

We report the case of a 70-year-old woman with ST-segment elevation myocardial infarction of the anterior wall, complicated by ventricular septal rupture (two septal defects--VSDs) with symptoms of cardiogenic shock. After 6 weeks of conservative treatment with inotropes and intra-aortic balloon support, the patient underwent surgical repair of VSDs with good clinical outcome.

Role of intramural platelet thrombus in the pathogenesis of wall rupture and intra-ventricular thrombosis following acute myocardial infarction.

Left ventricular thrombus (LVT) and rupture are important mechanical complications following myocardial infarction (MI) and are believed to be due to unrelated mechanisms. We studied whether, in fact, wall rupture and LVT are closely related in their pathogenesis with intramural platelet thrombus (IMT) playing a pivotal role. Male 129sv and C57Bl/6 mice underwent operation to induce MI, and autopsy was performed to confirm rupture deaths. Haemodynamic features of rupture events were monitored by telemetry in conscious mice. Detailed histological examination was conducted with special attention to the presence of IMT in relation to rupture location and LVT formation. IMT was detected in infarcted hearts of 129sv (82%) and C57Bl/6 (39%) mice with rupture in the form of a narrow streak spanning the wall or an occupying mass dissecting the infarcted myofibers apart. IMT often contained dense inflammatory cells and blood clot, indicating a dynamic process of thrombus formation and destruction. Notably, IMT was found extending into the cavity to form LVT. Haemodynamic monitoring by telemetry revealed that rupture occurred either as a single event or recurrent episodes. Importantly, the anti-platelet drug clopidogrel, but not aspirin, reduced the prevalence of rupture (10% vs. 45%) and IMT, and suppressed the degree of inflammation. Thus, IMT is a key pathological element in the infarcted heart closely associated with the complications of rupture and LVT. IMT could be either triggered by a wall tear or act as initiator of rupture. IMT may propagate towards the ventricular chamber to trigger LVT.

Post-infarct ventricular septal defect following thrombolytic intracranial bleed.

Mechanical complications after myocardial infarction are uncommon with advances in medical reperfusion strategies. However, such strategies are associated with bleeding complications which typically contraindicate surgical management. We describe a patient with a post-infarction ventricular septal defect and an intraventricular hemorrhage following thrombolytic therapy for an acute myocardial infarction.

Ventricular double rupture case of long-term survival without surgical repair.

A 78-year-old asymptomatic male with a history of coronary artery disease was admitted for preoperative cardiovascular evaluation before noncardiac surgery. Auscultation revealed a Grade 3 holosystolic murmur at the left parasternal area. Transthoracic echocardiography documented ventricular double rupture (VDR), consisting of ventricular septal rupture, and rupture of the apical part of the left ventricular free wall with pseudoaneurysm formation. Hospital records revealed that VDR had been noticed 7 years ago during hospitalization due to anterior myocardial infarction. However, recommended surgical repair could not be performed because of the patient's refusal.

Infarction-exclusion technique with the on-pump beating heart approach for ventricular septal perforation.

We report a successful surgical management of postinfarction ventricular septal perforation by infarction-exclusion technique with the on-pump beating heart approach and concomitant coronary artery bypass grafting. The identification of the suture line by direct inspection and finger palpation could be more accurate in determining contractile, thus viable myocardium supporting the patch, and concomitant coronary artery bypass grafting with on-pump beating heart could minimize the cardioplegia-induced myocardial damage.

Transcatheter closure of postinfarction ventricular septal defect using the Amplatzer atrial septal defect occluder.

Rupture of the interventricular septum is a rare and life-threatening complication of acute myocardial infarction. Postmyocardial infarction, ventricular septal defect is associated with very high morbidity and mortality. The therapy of this complication is the surgical closure. The Amplatzer occluder is currently used to close percutaneously atrial septal defect, patent foramen ovale, and selected congenital ventricular septal defect. Few cases are described regarding transcatheter closure of a postinfarction ventricular septal defect. Here we report a case of a large postinfarction ventricular septal defect successfully closed with Amplatzer multifenestrated atrial septal defect occluder device because of its peculiar anatomical characteristics.

Repair of ventricular septal perforation with asymmetrical conical patch exclusion.

We report a case of repair of the postinfarction ventricular septal perforation (VSP), using an equine pericardium tailored in an asymmetrical conical shape for exclusion (modified sack technique) and an additional direct patch closure of VSP. An asymmetrical conical patch is easily sutured to the normal septum away from the VSP edge by using the longer part of the cone border. The postoperative left ventriculogram 1.5 months after surgery revealed a minor leakage from the patch to the excluded left ventricle. However, no residual left to the right shunt was found in calculation from the oxygen saturation in blood samples. Echocardiography 1 year after surgery showed no residual patch leakage at all. We suggest that this modified sack technique is a simple and easy method by which to exclude the VSP.

Ventricular rupture secondary to cardiac metastasis of transitional cell carcinoma of the bladder.

We report a patient with transitional cell carcinoma of the bladder who had metastatic nodules in the myocardium of the left ventricle and tumour emboli in the left circumflex artery which caused myocardial infarction with ventricular rupture and haemopericardium. Cardiac metastasis of transitional cell carcinoma of the bladder is discussed and the literature reviewed.

Risk factors, echocardiographic patterns, and outcomes in patients with acute ventricular septal rupture during myocardial infarction.

Ventricular septal rupture (VSR), which can complicate an acute myocardial infarction (MI), carries a high mortality rate. Because precordial and transesophageal echocardiography can identify the type of rupture and assess right ventricular (RV) function at the patient's bedside, we examined the prognostic significance of echocardiographic patterns in postinfarct VSR by postulating that complex rupture and RV involvement carry a worse prognosis. Seventeen patients (10 men; mean age 66 years) who had confirmed postinfarct VSR underwent precordial and transesophageal echocardiography followed by coronary angiography. Serial 12-lead and right precordial leads were also available. Type of septal rupture was classified as simple or complex based on autopsy-proved echocardiographic criteria. Three patients had inferior wall MI and 14 had anterior wall MI. ST-segment elevation persisted >72 hours in all 3 patients who had inferior wall MI and in 12 who had anterior wall MI. Segmental wall motion abnormalities helped in detecting the left ventricular entry site, and use of unconventional views superimposed with color flow Doppler provided the RV exit site. RV function was better appreciated with transesophageal echocardiography. Two patients who had inferior wall MI and 7 who had anterior wall MI had complex ruptures. All 3 patients who had inferior wall MI and 7 who had anterior wall MI had electrocardiographic and echocardiographic evidence of RV involvement. Mortality rate was higher in patients who had complex rupture (78% vs 38%, p <0.001) and in those who had RV extension (71% vs 29%, p <0.001). In conclusion, persistent ST elevation is a common finding in patients who have postinfarct VSR. Complex VSR and RV involvement are significant determinants of clinical outcome.

Pathological findings of tissue reactivity of gelatin resorcin formalin glue: an autopsy case report of the repair of ventricular septal perforation.

A seventy-three-year-old man was treated for ventricular septal perforation with Gelatin Resorcin Formalin (GRF) glue. The patient died of multiple organ failure 36 days after the surgery. In autopsy, macroscopically, the inferior wall was reconstructed successfully by the GRF glue. Furthermore, microscopic study revealed the excellent growth of collagen and elastic fiber where the GRF was glued. No infiltration of inflammatory cells was evident. There have been no reports that the safety and efficacy of GRF glue was pathologically proven in an autopsy case.

Postmortem evaluation of morphologic changes in the infarcted myocardium that predict ventricular septal rupture in acute anteroseptal infarction.

Although thinning of the ventricular wall due to infarct expansion (septal aneurysm) may contribute to ventricular septal rupture (VSR), spatial factors predisposing to this mechanical complication have not been fully demonstrated. To identify the morphologic predictors of VSR, a retrospective postmortem study was performed on 17 hearts with acute anteroseptal myocardial infarction, comprising 7 with VSR and 10 without rupture. Infarct size and the extent of wall thinning were quantified. Wall thinning was defined as a decrease of less than 50% of thickness of the noninfarcted wall. The total infarct size did not differ among the groups. In the free wall (FW), the infarct was smaller in hearts with VSR than in those with a ruptured FW (p<0.05) or no rupture (p<0.01). The septal involvement was more extensive in patients with VSR than in those with FW rupture (p<0.05). Septal thinning was more extensive in hearts with VSR than in those with FW rupture (p<0.05) or non-rupture (p<0.05). A combination of a small infarct of the FW and a large septal infarct may contribute to the formation of septal aneurysm, which is believed to predispose to VSR. The presence of a small infarct of the anterior septum may be another setting for postinfarction septal rupture.