scholarly journals P626 Peripartum cardiomyopathy with persistent ventricular dysfunction and intracavitary thrombosis despite treatment with dopamine receptors agonist. The role of the three-dimensional echocardiography

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
Z Y Vasquez-Ortiz ◽  
R Gonzalez-Varela ◽  
J Navarrete Garcia ◽  
P Hernandez-Reyes ◽  
J Oseguera Moguel

Abstract Introduction Peripartum cardiomyopathy (MPP) is a type of cardiomyopathy characterized by heart failure secondary to left ventricular systolic dysfunction during the last month of pregnancy or in the first 5 months of puerperium without other apparent etiology, being a diagnosis of exclusion. The left ventricle is not always dilated, but the fraction of left ventricular ejection is always less than 45%. The natural history and prognosis of the disease is diverse. Ventricular dysfunction is usually transient and normalizes at 3-6 months in up to 60% of cases. Mortality is variable, with reports ranging from 0 to 28%, affecting more certain ethnic groups, in patients with persistent ventricular dysfunction, evidence of the efficacy of a specific treatment beyond optimal medical therapy for heart failure is limited. Clinical case We present the clinical case of a 22-year-old woman, who was referred to the our institute with an acute heart failure syndrome two months after the end of her first pregnancy. On admission to the hospital, dilated cardiomyopathy and intracavitary thrombi were documented by transthoracic echocardiography (TTE) with dilatation and eccentric left ventricular hypertrophy, generalized hypokinesia and mobile thrombi inside, the largest of 34x16mm with severe left ventricular dysfunction 3D LVEF of 28% and global longitudinal strain (GLS) of -5.8%, pulmonary hypertension and right ventricular dysfunction with severe functional tricuspid regurgitation. Other specific etiologies of dilated cardiomyopathy were investigated and discarded, finally establishing the diagnosis of peripartum cardiomyopathy. The support management was carried with inotropic, diuretic, supplemental oxygen and parenteral anticoagulation was initiated, with gradual improvement. Subsequently, optimal medical treatment was started for heart failure, cabergoline and vitamin K antagonist. He was released to his home on II NYHA. Two months later she presented with progressive dyspnea, increased abdominal perimeter. On March 14, 2018, a TTE was performed, with absence of improvement in conventional and advanced ventricular function parameters. Apical thrombi of smaller size compared with previous study, severe left ventricular dysfunction, which worsened with respect to the previous echocardiogram, with 3D LVEF of 25% and GLS 3.7% Discussion We present the case of a woman with MPP, in whom persistent left ventricular dysfunction after 6 months of diagnosis, although cabergoline scheme in addition to optimal medical management for heart failure, with no improvement. In patients who dont present an adequate response to the management, it is necessary to consider enlisting for heart transplantation. Abstract P626 Figure. TTE, severe ventricular dysfunction

2021 ◽  
Vol 31 (2) ◽  
pp. 391-394
Author(s):  
Andreea Elena VELCEA ◽  
Maria Claudia Berenice SURAN ◽  
Dragos VINEREANU

Tachycardia-induced cardiomyopathy (TIC) is characterized by reversible left ventricular dysfunction caused by long-standing tachycardia. Treatment options for tachyarrhythmias causing TIC have evolved, especially the rhythm control strategies, ensuring a better and more sustainable control of the arrhythmia. We report the case of a 46-year-old male presenting with acute heart failure, atrial fi brillation (AF) of unknown duration and severe left ventricular dysfunction, as well as left ventricular dilation. His medical history was relevant for atrial fl utter treated with catheter ablation, hypertension, and frequent atrial ectopy for which he had been prescribed amiodarone. Coronary artery disease and other potential causes for left ventricular dysfunction were excluded with coronary angiography and cardiac magnetic resonance. Thus, the patient had a high suspicion of TIC. We opted for a rhythm control strategy, however, after a successful initial electrical cardioversion, he had AF recurrence a few days later, under classic heart failure medication and antiarrhythmics. Pulmonary vein isolation was then performed, with no complications. At the one-month follow-up visit the patient was arrhythmia-free and had a normal left ventricular ejection fraction, with a slightly enlarged left ventricle. We opted to continue the heart failure medication. This case illustrates a typical case of AF induced TIC and the limited pharmacological options that exist for rhythm control, as well as the high efficacy of catheter ablation and value of imaging.


2014 ◽  
Vol 3 (1) ◽  
pp. 20-24 ◽  
Author(s):  
Khang-Li Looi ◽  
Anthony SL Tang ◽  
Sharad Agarwal

Current guidelines recommend cardiac resynchronisation therapy (CRT) for patients with severe left ventricular dysfunction (left ventricular ejection fraction [LVEF] ≤35 %), QRS duration of ≥120–150 ms (Class IA and IB indications) on surface electrocardiogram (ECG) and New York Heart Association (NYHA) class III or IV heart failure (HF) symptoms. Ongoing studies aim to expand the use of CRT in patients with asymptomatic or minimal symptoms left ventricular dysfunction. There have been studies that have shown benefit of CRT extended to this group of patients. There have also been different implications of the role of CRT in patients with atrial fibrillation (AF), patients with narrow QRS duration or with right bundle branch block (RBBB) on surface ECG, as well as patients with end-stage renal failure on dialysis therapy. This article aims to review the current body of evidence of expanding use of CRT in these populations.


Heart ◽  
2017 ◽  
Vol 104 (12) ◽  
pp. 971-977 ◽  
Author(s):  
Peter A Henriksen

Anthracycline chemotherapy causes dose-related cardiomyocyte injury and death leading to left ventricular dysfunction. Clinical heart failure may ensue in up to 5% of high-risk patients. Improved cancer survival together with better awareness of the late effects of cardiotoxicity has led to growing recognition of the need for surveillance of anthracycline-treated cancer survivors with early intervention to treat or prevent heart failure. The main mechanism of anthracycline cardiotoxicity is now thought to be through inhibition of topoisomerase 2β resulting in activation of cell death pathways and inhibition of mitochondrial biogenesis. In addition to cumulative anthracycline dose, age and pre-existing cardiac disease are risk markers for cardiotoxicity. Genetic susceptibility factors will help identify susceptible patients in the future. Cardiac imaging with echocardiographic measurement of global longitudinal strain and cardiac troponin detect early myocardial injury prior to the development of left ventricular dysfunction. There is no consensus on how best to monitor anthracycline cardiotoxicity although guidelines advocate quantification of left ventricular ejection fraction before and after chemotherapy with additional scanning being justified in high-risk patients. Patients developing significant left ventricular dysfunction with or without clinical heart failure should be treated according to established guidelines. Liposomal encapsulation reduces anthracycline cardiotoxicity. Dexrazoxane administration with anthracycline interferes with binding to topoisomerase 2β and reduces both cardiotoxicity and subsequent heart failure in high-risk patients. Angiotensin inhibition and β-blockade are also protective and appear to prevent the development of left ventricular dysfunction when given prior or during chemotherapy in patients exhibiting early signs of cardiotoxicity.


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