Heart Rate Reduction with Ivabradine Prevents Cardiac Rupture after Myocardial Infarction in Mice.

PURPOSE: Cardiac rupture is a fatal complication following myocardial infarction (MI). An increase in heart rate (HR) is reportedly an independent risk factor for cardiac rupture during acute MI. However, the role of HR reduction in cardiac rupture after MI remains to be fully elucidated. We aimed to evaluate the therapeutic efficacy of HR reduction with ivabradine (IVA) on post-MI cardiac rupture in mice. METHODS: We induced MI in mice by ligating the left anterior descending coronary artery. Subsequently, we subcutaneously implanted osmotic pumps filled with IVA solution or vehicle (Veh) in the surviving MI mice at 24 h postoperatively. We biochemically analyzed the myocardium on day 5, additionally observed the mice for 10 days, and analyzed the rates of cardiac rupture and non-cardiac rupture death, and survival after MI. RESULTS: HR was significantly lower in the IVA-treated mice, whereas blood pressure was comparable between the two groups. Compared to the Veh-treated mice, apoptosis was significantly reduced in the MI border zone in the IVA-treated mice. Although there were no differences in the infarct size of the surviving MI mice between the two groups, HR reduction with IVA significantly reduced cardiac rupture (rupture rate 26 and 8% in the Veh-treated and IVA-treated groups, respectively) and improved survival after MI. CONCLUSION: Our findings suggest that HR reduction with IVA prevents cardiac rupture after MI. This may be particularly effective in MI patients with a high HR who are either unable to adequately tolerate ß-blockers or whose HR remains high despite receiving ß-blockers.

Curious case of calciphylaxis leading to acute mitral regurgitation.

Calciphylaxis is uncommon and typically seen in patients with end-stage renal disease. It has been defined as a vasculopathic disorder characterised by cutaneous ischaemia and necrosis due to calcification, intimal fibroplasia and thrombosis of pannicular arterioles. We present the case of a 74-year-old woman with chronic kidney disease stage III who developed calciphylaxis leading to mitral valve calcification, chordae tendineae rupture and acute mitral regurgitation. Although an alternative explanation can typically be found for non-uraemic calciphylaxis, her evaluation did not reveal any usual non-uraemic causes including elevated calcium-phosphorus product, hyperparathyroidism, or evidence of connective tissue disease. Her wounds improved with sodium thiosulfate, pamidronate, penicillin and hyperbaric oxygen therapies but she ultimately decompensated with the onset of acute mitral regurgitation attributed to rupture of a previously calcified chordae tendineae. This case highlights an unusual case of calciphylaxis without clear precipitant as well as a novel manifestation of the disease.

Perforation of the left ventricle due to an abscess of a left ventricular thrombus: survival of the patient with a conservative medical therapy strategy.

A 73-year-old male was admitted due to sepsis with fever up to 40°C after haemorrhoidectomy. Blood cultures identified Staphylococcus haemolyticus. In 1986 he developed left ventricular aneurysm containing an apical thrombus after anterior wall myocardial infarction. In 1994 aorto-coronary bypass grafting was performed without thrombus removal. Echocardiography on admission showed a thrombus formation in the apical aneurysm. In the thrombus an inhomogeneous floating structure in terms of an abscess was identified. Later, a small perforation occurred at the border of the thrombus. Vancomycin and Tygacil were given for 20 days. Repeated echocardiographies showed a thrombus liquefaction and disaggregation after 12 days. Finally, a territorial haemopericardium with residual thrombus developed. Infection of a ventricular thrombus by septicaemia with myocardial wall infiltration by haemolysing Staphylococcus is rare but can result in spontaneous ventricle perforation. The patient survived and is after 18 months alive suffering form heart failure NYHA class II-III.

Administration of intrapericardial tissue adhesive after cardiac rupture and cardiac tamponade.

OBJECTIVE: To describe a series of patients treated with intrapericardial glue. DESIGN: Case reports. Descriptive study. PATIENTS: We describe the results obtained using the injection of a surgical intrapericardial adhesive in 19 patients who presented cardiac tamponade and shock after cardiac rupture. The technique was done using puncture and echocardiographic subxiphoid control. At the one-year follow-up, 5 patients had survived, with neither pseudoaneurysms nor constriction. One patient was injected with said adhesive in the right ventricular cavity. CONCLUSIONS: Pericardial drainage, followed by the administration of intrapericardial glue may be an attractive technique. This technique should be studied for its possible utility when faced with surgical impossibility.

Oozing type cardiac rupture repaired with percutaneous injection of fibrin-glue into the pericardial space: case report.

Two patients, a 56-year-old man and an 81-year-old woman who were admitted to hospital because of anteroseptal acute myocardial infarction, were initially treated successfully with direct percutaneous transluminal coronary angioplasty. However, both patients later developed sudden cardiogenic shock due to cardiac tamponade caused by left ventricular free wall rupture (LVFWR). Prompt, life-saving pericardiocentesis was performed, then fibrin-glue was percutaneously injected into the pericardial space. After the procedure, there was no detectable pericardial effusion on echocardiography and the hemodynamic state became stable. The surgical treatment was the standard procedure for LVFWR, but percutaneous fibrin-glue therapy can also be considered for oozing type LVFWR.

Effect of nitroglycerin and ibuprofen on left ventricular topography and rupture threshold during healing after myocardial infarction in the dog.

The effect of nitroglycerin and ibuprofen, given between 2 and 7 days after left anterior descending coronary artery ligation, on the mechanical resistance of the infarcted left ventricle to rupture or the rupture threshold (balloon technique), and on topography (computerized planimetry) and function (two-dimensional echocardiography) at 7 days (n = 32) and 42 days (n = 34) postligation was studied in 66 dogs randomly allocated to sham (no infarction, n = 22) and infarction subgroups (15 controls; 15 received nitroglycerin, 30 mg oral isosorbide dinitrate b.i.d.; 14 received ibuprofen, 200 mg t.i.d. orally). Nitroglycerin decreased mean arterial and left atrial pressures, decreased diastolic cross-sectional area, and improved systolic function, while ibuprofen increased diastolic area. Infarction subgroups showed infarct shrinkage and more infarct hydroxyproline at 6 weeks. Compared with shams, all infarct subgroups showed early expansion and thinning, with further marked late thinning in controls. Nitroglycerin produced less expansion and thinning both at 1 and 6 weeks, while ibuprofen produced marked early thinning. Rupture threshold was less at 6 weeks than 1 week with controls and ibuprofen but remained unchanged with nitroglycerin. Passive prerupture stiffness was less at 6 weeks than at 1 week in controls but remained unchanged with nitroglycerin and ibuprofen. Thus, reduced expansion and thinning with nitroglycerin during the first week after infarction improved function, mechanical strength, and resistance to distension at 6 weeks.

Subacute left ventricular free wall rupture following acute myocardial infarction: bedside hemodynamics, differential diagnosis, and treatment.

Six patients with subacute left ventricular free wall rupture (anatomically proved) following acute myocardial infarction are presented. Diagnosis of cardiac rupture in every case was suspected several hours before death or surgical intervention, when clinical and hemodynamic data of cardiac tamponade were found. In three patients right atrial pressure decreased with inspiration and in the other three cases it did not show any modification. These latter three patients had associated right ventricular infarction; the abnormal respiratory behavior could be explained by restriction produced by a noncompliant right ventricle. All six patients improved initially with medical treatment (inotropics and fluid infusion) and three of them were operated upon. One of the latter patients died on the eighteenth postoperative day of extracardiac causes and two are long-term survivors.

Treatment of ruptured interventricular septum with afterload reduction.

Two patients with a ruptured interventricular septum complicating acute myocardial infarction were treated with isosorbide dinitrate. The first patient recovered from cardiogenic shock after sublingual administration of 5 mg of isosorbide dinitrate every two hours and was successfully operated on. The second patient recovered from severe pulmonary edema during the acute stage of the infarction with sublingual isosorbide dinitrate. Moreover, she experienced a considerable symptomatic improvement when a 5 mg sublingual dose of isosorbide dinitrate every three hours was added to her long-term treatment. Analysis of hemodynamic data showed that the most striking change following administration of the drug was the substantial reduction of pulmonary wedge pressure. The striking symptomatic and hemodynamic improvement was achieved by the favorable effect of afterload reduction on left ventricular performance and not by reduction in left to right shunt.