scholarly journals Zinc Deficiency as a Reversible Cause of Heart Failure

2020 ◽  
Vol 47 (2) ◽  
pp. 152-154
Author(s):  
Hannah Rosenblum ◽  
Behnood Bikdeli ◽  
Jeffrey Wessler ◽  
Aakriti Gupta ◽  
Daniel Louis Jacoby

Zinc, an essential micronutrient, affects the heart by modulating cardiomyocyte oxidative stress and maintaining myocardial structure, among other mechanisms. In cross-sectional studies, patients with heart failure have often had zinc deficiencies, suggesting effects on the ongoing pathogenesis of heart failure. Low plasma and myocardial zinc levels may cause reversible cardiomyopathy in patients who have nutritional deficiencies. We present the case of a 24-year-old woman with anorexia nervosa and new-onset heart failure whose depressed left ventricular systolic function improved after zinc supplementation. To our knowledge, this is the first report of low plasma zinc levels as the chief cause of cardiomyopathy that resolved after zinc supplementation.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Theophilus Owan ◽  
Kimberly Morley ◽  
Travis G Ault ◽  
Ronny Jiji ◽  
Nathaniel Hall ◽  
...  

Background: Obesity is associated with an increased risk of developing heart failure. Based on cross sectional studies, it has been hypothesized that the duration of obesity is the key factor leading to impaired cardiac function. However, longitudinal data to confirm this hypothesis are not available. Methods: We prospectively studied 62 severely obese patients at baseline, 2 and 5 years after randomization to nonsurgical therapy (NonSurg, n = 25) or Rouxen-Y gastric bypass surgery (GBS, n = 37). Echocardiography was used to measure left ventricular (LV) size and ejection fraction (EF). Results: At enrollment, the mean BMI was 46±9 and the mean age was 47±11 years (range 25– 66). GBS subjects lost 96± 26 vs. 6±18 lbs at 2 years and 78±42 vs. 17±42 lbs at 5 years compared to NonSurg (p<0.0001 for both). At baseline LVEF was not different between GBS and nonsurg (67±9 vs. 64±8%) and it did not change at 2 years (64±9 vs. 63±9%) or 5 years (63±9 vs. 63±10%). LV diastolic dimension did not change over time in control (4.3±1.0 vs. 4.2±0.6 vs. 4.5±0.3) or GBS patients (4.4±0.6 vs. 4.3±0.7 vs. 4.4±0.4). Stratifying the entire group by quartiles of age or duration of obesity (quartile 1 avg duration = 16 years, quartile 4 average duration = 56 years), we found no evidence of time-dependent changes in LV size or function. Conclusion: In this, prospective study of severely obese patients we found no evidence of progressive changes in LV size or EF over a period of 5 years. Moreover, we find no relationship between age or duration of obesity and LV size or LVEF. These data argue strongly that other factors such as the development of coronary disease are the most likely causes of heart failure in obese patients.


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