Michael J. Ackerman works in Electrophysiology affiliated with Mayo Clinic.
Michael J. Ackerman, M.D., Ph.D., is a pediatric cardiologist at Mayo Clinic in Rochester, Minnesota. He serves as professor of medicine, pediatrics, and pharmacology, and directs the Windland Smith Rice Sudden Death Genomics Laboratory and the Long QT Syndrome/Inherited Arrhythmia Clinic. His research focuses on genomics and genotype-phenotype relationships in heritable cardiovascular diseases predisposing to sudden death.
1,422 pubs · 80,398 cites · h-index 153
MD/PhD
Mayo Clinic College of Medicine
1995
BA Chemistry and Mathematics
Luther College
1988
Consultant, Division of Heart Rhythm Services, Department of Cardiovascular Medicine
Mayo Clinic
Consultant, Division of Pediatric Cardiology, Department of Pediatrics
Mayo Clinic
Consultant, Department of Molecular Pharmacology and Experimental Therapeutics
Mayo Clinic
Professor of Medicine, Pediatrics, and Pharmacology
Mayo Clinic College of Medicine
Specialty-center LQTS management yields low BCE rates; leaves open optimization needs for the 25% of symptomatic patients with subsequent events.
Infants with LQTS who survive an aborted cardiac arrest in the first year of life are at extremely high risk (HR 23.4) for recurrent arrest or sudden death before age 10, and beta-blocker monotherapy appears insufficient to protect this high-risk subset.
Supports AI-ECG evaluation for pediatric HCM detection; leaves open prospective validation before screening use.
Cardiologist, Amsterdam University Medical Centers · Amsterdam University Medical Centers
to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate specific experience.
Journal of the American College of CardiologyBains et al.
Cardiologist and Director, Baker Heart and Diabetes Institute · Baker Heart and Diabetes Institute
The current paper confirms these findings in a larger group, shows that EMW outperformed QTc in predicting symptomatic patients (area under the curve: 0.78 vs. 0.70; p = 0.01), and confirms that EMW increases as the number of genetic abnormalities increases but was not clearly linked to a particular genotype. Importantly, it confirms the reliability of measuring this signal at routine echocardiography, with an intraclass correlation coefficient (ICC) of 0.93 (95% confidence interval: 0.89 to 0.96) among 22 sonographers who underwent a short training process.
Journal of the American College of CardiologySugrue et al.
Provides the first dedicated framework for tactical athletes; extends prior competitive sports cardiology guidance to occupational high-risk settings.
Ventricular arrhythmia risk appears comparable across titin truncating variant phenotypes; leaves open arrhythmia surveillance needs in phenotype-negative carriers pending prospective data.
Transmural LGE may identify higher-risk genotype-positive cardiomyopathy patients; leaves open its incremental value for risk stratification or management decisions.
May warrant closer monitoring in multiple-variant carriers; extends single-study evidence but leaves open therapeutic implications.
DENND3-p.R534S promotes arrhythmia in iPSC-CMs via microdomain disruption; hypothesis-generating for Rab11b inhibition in VF, not yet for clinical use.
May support immunomodulatory strategies in DSP cardiomyopathy; leaves open whether this alters progression or arrhythmias.
AI-ECG sex/age signals in athletes should not change screening; leaves open validation for low EF, HCM, or AF detection.
Secondary ICa,L remodeling may amplify LQT2 repolarization defects; hypothesis-generating for combined channel blockade in patient-derived models.
The JPH2 E169K mutation causes atrial fibrillation by impairing RyR2 stabilization, highlighting a novel mechanism of arrhythmogenesis and a potential therapeutic target.
May support flecainide for exercise-related ectopy in PKP2-ACM; hypothesis-generating and requires prospective confirmation.
Exercise-induced accentuation of J-point elevation identifies a subset of Brugada syndrome patients at significantly higher risk for exertional cardiac events.
