BackgroundAs heart failure (HF)‐associated morbidity and mortality continue to escalate, enhanced focus on prevention is increasingly important. “Malignant” left ventricular (LV) hypertrophy (LVH): LVH combined with an elevated cardiac biomarker reflecting either injury (high‐sensitivity cardiac troponin T), or strain (amino‐terminal pro‐B‐type natriuretic peptide) has predicted accelerated progression to HF. We sought to determine whether malignant LVH identified community‐dwelling adults initially free of cardiovascular disease at high risk of asymptomatic decline in LV ejection fraction or a clinical cardiovascular event.Methods and ResultsA total of 4985 of 6814 individuals without prevalent cardiovascular disease underwent baseline cardiac magnetic resonance for LVH in combination with measurement of plasma high‐sensitivity cardiac troponin T and amino‐terminal pro‐B‐type natriuretic peptide as part of MESA (Multi‐Ethnic Study of Atherosclerosis) and were subsequently divided into 4 groups: (1) No LVH, no elevated biomarkers (n=2206; 44.3%); (2) No LVH, ≥1 elevated biomarkers (n=2275; 45.7%); (3) LVH, no elevated biomarkers (n=153; 3.0%); and (4) LVH, ≥1 elevated biomarkers (malignant LVH; n=351; 7.0%). Cardiac magnetic resonance was repeated 10 years later (n=2831) for assessment of LV ejection fraction <50%. Median follow‐up was 12.2 years. Malignant LVH was associated with 7.0‐, 3.5‐, and 2.6‐fold adjusted increases in incidence of HF, cardiovascular death, and asymptomatic LV dysfunction, respectively, versus group 1. New‐onset HF was predominately HF with reduced ejection fraction (9.5‐fold increase).ConclusionsMalignant LVH is predictive of progression to asymptomatic LV dysfunction, HF (particularly HF with reduced ejection fraction), and cardiovascular death. Consequently, malignant LVH represents a high‐risk phenotype among individuals without known cardiovascular disease, which should be targeted for increased surveillance and more‐aggressive therapies.

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Introduction: The worldwide first genetically modified porcine-to-human cardiac xenotransplantation was performed in January 2022 at the University of Maryland with the recipient surviving for 61 days. Methods: Daily 12- lead ECGs were obtained during the post-operative period. Results: Accepted “pig heart-in-pig body” ECG parameters demonstrate a short PR interval (50-120ms), short QRS (70-90ms) and short QT (260-380ms). However, the first-ever EKG of a genetically modified heart xenotransplant (“pig heart-in-human body”) demonstrated a relatively longer PR interval of 190ms, QRS duration of 138ms and QT of 538ms (in setting of sinus bradycardia, interventricular conduction delay and inferior/antero-lateral T wave inversions; Figure 1). Prolonged intrinsic PR intervals remained stable during the post-operative course with 210±22ms [range 142-246ms]. However, atrial pacing demonstrated evidence of decremental intra-atrial conduction delay/AV-conduction delay most pronounced on day 12 (PR: 380ms). QRS duration remained prolonged with 145±16ms [range 116-192ms] but shortened during the post-operative course (day 21-40 vs 41-60: 148±14ms vs 132±11ms; p<0.001). Increased QT persisted with 509±54ms [range 384-650ms] with dynamic fluctuations (QT nadir around day 14 (428±22ms vs 533±36ms; p<0.001). Conclusions: ECG parameters of the first genetically modified porcine-to-human cardiac xenotransplant (“pig heart-in-human body”) demonstrated prolongation over the usually encountered ECG measurements in the donor (“pig heart- in-pig body”) including changes in cardiac depolarization and repolarization. Prolonged ECG parameters persisted but showed dynamic changes during post-operative period. This provides a first insight into the novel and evolving field of xenotransplanation suggesting a complex interplay of inter-species physiology and porcine denervation in addition to post-surgical and medication-related changes.

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