The association between thyroid hormones and cardiovascular conditions has been well studied, specifically, the effects of hypothyroidism on cardiomyopathy, and hyperthyroidism with arrhythmias. Nonetheless, an explicit correlation between hyperthyroidism and cardiomyopathy has yet to be established. Medical databases MEDLINE and PubMed were accessed and queried as primary sources for data acquisition. Search criteria consisted of "hyperthyroidism", "heart failure", and "thyroid and cardiovascular system", which allowed the retrieval of relevant and recent works. From these sources, a consensus was developed and employed to yield an updated review of the etiology of heart failure in the setting of hyperthyroidism. It is rare for patients with hyperthyroidism to remain in a chronic hyperthyroid state, making it difficult to analyze subsequent long-term effects on the cardiovascular system. Related to heart failure, some studies have demonstrated no change in ejection fraction, while others have shown an acute change along with diastolic dysfunction, with or without an underlying rhythm abnormality. Further investigation is warranted to elucidate the mechanism driving such cardiac dysfunction, and whether it is due to vascular changes, tachyarrhythmias, or myocyte remodeling and fibrosis. The intent of this review article is to improve our understanding of how a hyperthyroid state affects cardiovascular function. An enhanced understanding of the effects on cardiovascular physiology will afford physicians the ability to provide more comprehensive care in consideration of both endocrine and cardiovascular pathologies.

IntroductionSacubitril/valsartan (SV) promotes cardiac remodeling and improves prognosis in patients with heart failure (HF). However, the response to the drug may vary between patients and its implementation in daily clinical practice has been slower than expected. Our objective was to develop a score predicting the super-response to SV in HF outpatients.MethodsThis is a retrospective analysis of 185 consecutive patients prescribed SV from two tertiary hospitals between September 2016 and February 2018. Super-responder was defined as a patient taking the drug and (i) without HF admissions, death, or heart transplant, and (ii) with a ≥50% reduction in NT-proBNP levels and/or an increase of ≥10 points in LVEF in a 12-month follow-up period after starting SV. Clinical, echocardiographic, ECG, and biochemical variables were used in a logistic regression analysis to construct a score for super-response to SV which was internally validated using bootstrap method.ResultsOut of 185 patients, 65 (35%) fulfilled the super-responder criteria. Predictors for super-response to SV were absence of both previous aldosterone antagonist and diuretic treatment, NYHA I-II class, female gender, previous 1-year HF admission, and sinus rhythm. An integrating score distinguished a low- (<25%), intermediate- (∼46%), and high-probability (>80%) for 1-year super-response to SV. The AUC for the model was 0.72 (95%CI: 0.64–0.80), remaining consistent after internal validation.ConclusionOne-third of our patients presented a super-response to SV. We propose an easy-to-calculate score to predict super-response to SV after 1-year initiation based on variables that are currently assessed in clinical practice.