Staged transcatheter closure of chronic postinfarction ventricular septal defects with the Amplatzer septal occluder

Ventricular septal rupture is a serious complication of myocardial infarction with an extremely poor outcome. There are single reports of transcatheter closure of postmyocardial septal defects and clinical experience is limited. This paper reports on a successful staged transcatheter closure of two chronic postmyocardial defects using the Amplatzer septal occluder in a 52-year-old male.     

Successful invasive management and surgical repair of subacute ventricular rupture complicating myocardial infarction

We describe a patient following acute myocardial infarction with a protracted clinical course presenting transient episodes of hypotension, who eventually developed cardiac tamponade. Echocardiography demonstrated pericardial effusion and emergency pericardiocentesis revealed blood. The patient's condition was stabilized and she underwent emergency thoracotomy with successful repair of left ventricular rupture. We discuss the literature and suggest an approach for management of patients with suspected ventricular rupture after myocardial infarction.     

Neurohormones in an ovine model of compensated postinfarction left ventricular dysfunction

Clinical heart failure, often the result of myocardial infarction, may be preceded by a period of compensated left ventricular impairment. There is substantial need for an experimental model that reflects this human condition. In sheep, coronary artery ligation produced consistent left ventricular anteroapical myocardial infarctions resulting in chronic (5 wk), stable hemodynamic changes compared with sham controls, including reductions in ejection fraction (51 +/- 2 vs. 30 +/- 5%, P < 0.001), cardiac output (6.3 +/- 0.2 vs. 5.1 +/- 0.2 l/min, P < 0.01), and arterial pressure (93 +/- 2 vs. 79 +/- 3 mmHg, P < 0.001), and increases in cardiac preload (left atrial pressure, 3.3 +/- 0.1 vs. 8.3 +/- 1.3 mmHg, P < 0.001). These changes were associated with acute and sustained increases in plasma concentrations of atrial natriuretic peptide (ANP; 5 wk, 11 +/- 2 vs. 27 +/- 5 pmol/l, P < 0.001), brain natriuretic peptide (BNP; 3 +/- 0.2 vs. 11 +/- 2 pmol/l, P < 0.001), and amino-terminal pro-brain natriuretic peptide (NT-BNP; 17 +/- 3 vs. 42 +/- 12 pmol/l, P < 0.001). Significant correlations were observed between plasma levels of the natriuretic peptides (ANP, day 7 to week 5 samples; BNP and NT-BNP, day 1 to week 5 samples) and changes in left ventricular volumes and ejection fraction. In contrast, renin activity, aldosterone, catecholamines, and endothelin were not chronically elevated postinfarction and were not related to indexes of ventricular function. Coronary artery ligation in sheep produces the pathological, hemodynamic, and neurohormonal characteristics of compensated left ventricular impairment secondary to myocardial infarction. Plasma concentrations of the cardiac natriuretic peptides are sensitive markers of left ventricular dysfunction. This is a reproducible model that reflects the clinical condition and should prove suitable for investigating the pathophysiology of, and experimental therapies in, early left ventricular dysfunction.     

Successful bystander cardiopulmonary resuscitation complicated by liver rupture

A 40-year-old man, who had collapsed while running and was resuscitated successfully by bystanders, was referred. An automated external defibrillator had shown ventricular fibrillation before a single shock restored sinus rhythm. On arrival, the patient was alert and haemo-dynamically stable. He reported that he had recently suffered from chest pain during exercise but had not visited his general practitioner; before collapsing he had no complaints. Physical examination showed a moderately tender abdomen with normal peristalsis.     

Right-sided endocarditis and ventricular septal defect.

Right-sided endocarditis occurred in a 40-year-old woman with ventricular septal defect. This association is uncommon in adults. Because of the changing and variable clinical patterns of this disease, it is difficult to make a prompt diagnosis. In this case diagnosis was delayed for almost a year. The occurrence of pneumonia due to Streptococcus viridans was the most important extracardiac manifestation.     

High-fat diet postinfarction enhances mitochondrial function and does not exacerbate left ventricular dysfunction

Lipid accumulation in nonadipose tissue due to enhanced circulating fatty acids may play a role in the pathophysiology of heart failure, obesity, and diabetes. Accumulation of myocardial lipids and related intermediates, e.g., ceramide, is associated with decreased contractile function, mitochondrial oxidative phosphorylation, and electron transport chain (ETC) complex activities. We tested the hypothesis that the progression of heart failure would be exacerbated by elevated myocardial lipids and an associated ceramide-induced inhibition of mitochondrial oxidative phosphorylation and ETC complex activities. Heart failure (HF) was induced by coronary artery ligation. Rats were then randomly assigned to either a normal (10% kcal from fat; HF, n = 8) or high saturated fat diet (60% kcal from saturated fat; HF + Sat, n = 7). Sham-operated animals (sham; n = 8) were fed a normal diet. Eight weeks postligation, left ventricular (LV) function was assessed by echocardiography and catheterization. Subsarcolemmal and interfibrillar mitochondria were isolated from the LV. Heart failure resulted in impaired LV contractile function [decreased percent fractional shortening and peak rate of LV pressure rise and fall (+/-dP/dt)] and remodeling (increased end-diastolic and end-systolic dimensions) in HF compared with sham. No further progression of LV dysfunction was evident in HF + Sat. Mitochondrial state 3 respiration was increased in HF + Sat compared with HF despite elevated myocardial ceramide. Activities of ETC complexes II and IV were elevated in HF + Sat compared with HF and sham. High saturated fat feeding following coronary artery ligation was associated with increased oxidative phosphorylation and ETC complex activities and did not adversely affect LV contractile function or remodeling, despite elevations in myocardial ceramide.     

Interaction between AT1 and AT2 receptors during postinfarction left ventricular remodeling

The relative contribution of the angiotensin II type 1 and 2 receptors (AT1-R and AT2-R) in postmyocardial infarction (MI) remodeling remains incompletely understood. We studied five groups of C57Bl/6 mice after 1 h of left anterior descending artery occlusion-reperfusion: 1) wild type, untreated (n = 12); 2) wild type, treated with the AT1-R blocker losartan (10-20 mg.kg(-1).day(-1) in drinking water) from day 1 to day 28 post-MI (n = 10); 3) cardiac overexpression of the AT2-R [AT2-transgenic (TG); n = 14]; 4) AT2-TG treated with losartan (n = 13); and 5) AT2-TG and null for the AT1a-R [AT2-TG/AT1 knockout (KO); n = 10]. Cardiac magnetic resonance imaging (CMR) measured ejection fraction and left ventricular end-diastolic and end-systolic volume (EDVI and ESVI) and mass indexed to weight on days 0, 1, 7, and 28 post-MI. Infarct size was measured on day 1 by late gadolinium-enhanced CMR. Regional myocyte hypertrophy and collagen content were measured on day 28 post-MI. Infarct size was similar among groups. Systolic blood pressure was lowest in AT2-TG/AT1KO. By day 28 post-MI, when corrected for baseline differences, EDVI and ESVI were higher and ejection fraction was lower in wild type than other groups. Ejection fraction was highest and EDVI and mass index were lowest in AT2-TG/AT1KO at day 28. The AT2-TG/AT1KO demonstrated less fibrosis in adjacent regions. Regional myocyte hypertrophy was similar in all groups. The AT1-R and AT2-R are intricately intertwined in post-MI remodeling. Pharmacological blockade of AT1-R is equivalent to AT2-R overexpression in attenuating post-MI remodeling. Genetic knockout of the AT1a-R is additive to AT2-R overexpression, due, at least in part, to blood pressure lowering.     

Percutaneous occlusion of post-myocardial infarction ventricular septum rupture

Aims

The aim of this systematic review is to gain insight into the published experience on percutaneous closure of a post-infarction ventricular septal rupture (VSR).

Method

Relevant literature was obtained by MeSH-term searches in the online search-engine PubMed. Articles published in the last 10 years were included. Further filtering was done by using search limits and individual article selection based on the aims of this systematic review.

Conclusion

Percutaneous closure is a potential technique in a select group of patients. The presence of cardiogenic shock and closure in the acute phase after VSR diagnosis are important risk factors of mortality. Device implantation is in general successful with few procedure-related complications. Reduction of the shunt fraction has been reported frequently. This technique is a less invasive alternative to surgical treatment and should be applied on a case-by-case basis.     

Heritable ventricular septal defect in Yucatan miniature swine

A heritable ventricular septal defect (VSD) was found in a strain of Yucatan miniature swine. The defect was determined to be a high membranous VSD analogous in anatomic location to the most common from of VSD in humans. Eighteen animals were studied clinically, hemodynamically and at necropsy to characterize the defect. Three mature animals developed pulmonary hypertension. Three animals were found to have a patent foramen ovale (PFO) in addition to the VSD. VSD is heritable probably due to polygenic factors. VSD in Yucatan miniature swine may be a suitable model of the human disease syndrome.     

Late ventricular fibrillation following successful resuscitation from postinfarction cardiogenic shock with intraaortic balloon pumping

Early ventricular fibrillation occurs in approximately 5% of patients admitted for acute myocardial infarction. Although late ventricular fibrillation (> 48 hours postinfarction) may occur in stable patients, it occurs more commonly when severe left ventricular power failure is present. We have encountered late ventricular fibrillation in three of 42 (7%) patients treated with intraaortic balloon pumping (IABP) for profound cardiogenic shock secondary to myocardial infarction. These patients progressed to our hemodynamic Class A prior to weaning, and were thought to be stable prior to IABP removal. They were the only ones who expired after achieving Class A status. The episodes of late ventricular fibrillation occurred after the patients had been successfully weaned from IABP and were free of arrhythmias. This experience suggests that prolonged antiarrhythmic therapy may be indicated for postinfarction patients who have had ventricular dysrhythmias during IABP support.