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
JACCRohatgi et al.cohort
Specialty-center LQTS management yields low BCE rates; leaves open optimization needs for the 25% of symptomatic patients with subsequent events.
JACCSpazzolini et al.cohort
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.
Heart RhythmCastrichini et al.Original Research
JACCSiontis et al.case-control
Supports AI-ECG evaluation for pediatric HCM detection; leaves open prospective validation before screening use.
Heart RhythmCoderre et al.Original Research
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.
JACCDineen et al.Guideline
This scientific statement from the ACC and AHA provides a framework for evaluating tactical athletes, including firefighters and military personnel, with or at risk for heart disease. It comprises 11 sections covering preparticipation screening, ethical aspects, and specific conditions like cardiomyopathies and arrhythmias. The document guides fit for full duty assessments by factoring in how a heart event might impact teammates, community safety, and mission success.
JACC. Clinical electrophysiologyCoderre et al.cohort
Ventricular arrhythmia risk appears comparable across titin truncating variant phenotypes; leaves open arrhythmia surveillance needs in phenotype-negative carriers pending prospective data.
JACC. Clinical electrophysiologyCastrichini et al.cohort
Transmural LGE may identify higher-risk genotype-positive cardiomyopathy patients; leaves open its incremental value for risk stratification or management decisions.
Heart RhythmNouraee et al.cohort
May warrant closer monitoring in multiple-variant carriers; extends single-study evidence but leaves open therapeutic implications.
EP EuropaceGao et al.preclinical
DENND3-p.R534S promotes arrhythmia in iPSC-CMs via microdomain disruption; hypothesis-generating for Rab11b inhibition in VF, not yet for clinical use.
Heart Rhythm O2Ezzeddine et al.Original Research
May support immunomodulatory strategies in DSP cardiomyopathy; leaves open whether this alters progression or arrhythmias.
JACCFatunde et al.Original Research
AI-ECG sex/age signals in athletes should not change screening; leaves open validation for low EF, HCM, or AF detection.
Circulation Arrhythmia and ElectrophysiologyHuynh et al.preclinical
Secondary ICa,L remodeling may amplify LQT2 repolarization defects; hypothesis-generating for combined channel blockade in patient-derived models.
JACCBeavers et al.preclinical
The JPH2 E169K mutation causes atrial fibrillation by impairing RyR2 stabilization, highlighting a novel mechanism of arrhythmogenesis and a potential therapeutic target.
EP EuropaceCastrichini et al.cohort
May support flecainide for exercise-related ectopy in PKP2-ACM; hypothesis-generating and requires prospective confirmation.
CirculationAl‐Khatib et al.Guideline
JACC. Clinical electrophysiologySardana et al.cohort
Exercise-induced accentuation of J-point elevation identifies a subset of Brugada syndrome patients at significantly higher risk for exertional cardiac events.
