scholarly journals Low voltage in limb leads in arrhythmogenic cardiomyopathy

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
S Peters

Abstract   Low voltage in limb leads characterizes left ventricular involvement in arrhythmogenic cardiomyopathy. A large collective of patients with arrhythmogenic cardiomyopathy including 438 patients (268 males, mean age 46.8±11.6 years) were analyzed. Method Low voltage in limb leads were analyzed in typical patients with arrhythmogenic cardiomyopathy. Several other ECG features such a slow voltage in precordial leads, epsilon waves, right precordial T wave inversions, QRS fragmentation, typical appearance in lead aVR, amplitude of T wave inversion in special right ventricular leads, and developing complete right bundle branch block. Results Low voltage in limb leads was found in 60 patients (15%). Two patients represented with low voltage in limb leads and T wave inversions in inferolateral leads charactizing arrhythmogenic left ventricular leads with moderate reduction of left ventricular function with a large aneurysm of the apex. The other patients presented with sustained RBBB-VT. In 38 patients low voltage in limb leads and typical ECG findings of arrhythmogenic cardiomyopathy were found. These patients had arrhythmogenic biventricular cardiomyopathy of moderate reduction of left ventricular function and typical arrhythmias. Low voltage in limb and precordial leads was found in 14 patients with two cardiac deaths due to therapy-resistant heart failure. In 6 cases low voltage in limb and precordial leads and developing complete right bundle branch block were found. Four patients were tranplanted, two cases died due to heart failure. These 20 patients characterize advances, end-stage disease arrhythmogenic cardiomyopathy. Conclusion Standard ECG can differentiate between arrhythogenic left ventricular, arrhythmogenic biventricular, and arrhythmogenic advanced end-stage cardiomyopathy FUNDunding Acknowledgement Type of funding sources: None.

Heart Rhythm ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. S148
Author(s):  
Ikutaro Nakajima ◽  
Kenichi Tokutake ◽  
Asad A. Aboud ◽  
Oluwaseun Adeola ◽  
Travis D. Richardson ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 396
Author(s):  
Wolf-Stephan Rudi ◽  
Michael Molitor ◽  
Venkata Garlapati ◽  
Stefanie Finger ◽  
Johannes Wild ◽  
...  

Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function and survival. We aimed to elucidate the impact of early treatment with the ACE inhibitor ramipril on the hematopoietic response after MI, as well as on the chronic systemic and vascular inflammation. Methods and Results: In a mouse model of MI, induced by permanent ligation of the left anterior descending artery, immediate initiation of treatment with ramipril (10 mg/k/d via drinking water) reduced cardiac inflammation and the number of circulating inflammatory monocytes, whereas left ventricular function was not altered significantly, respectively. This effect was accompanied by enhanced retention of hematopoietic stem cells, Lin−Sca1−c-Kit+CD34+CD16/32+ granulocyte–macrophage progenitors (GMP) and Lin−Sca1−c-Kit+CD150−CD48− multipotent progenitors (MPP) in the bone marrow, with an upregulation of the niche factors Angiopoetin 1 and Kitl at 7 d post MI. Long-term ACE inhibition for 28 d limited vascular inflammation, particularly the infiltration of Ly6Chigh monocytes/macrophages, and reduced superoxide formation, resulting in improved endothelial function in mice with ischemic heart failure. Conclusion: ACE inhibition modulates the myeloid inflammatory response after MI due to the retention of myeloid precursor cells in their bone marrow reservoir. This results in a reduction in cardiac and vascular inflammation with improvement in survival after MI.


2010 ◽  
Vol 28 ◽  
pp. e50-e51
Author(s):  
F Santi ◽  
ER Cosentino ◽  
D Degli Esposti ◽  
ER Rinaldi ◽  
S Bacchelli ◽  
...  

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