Shan S. Parikh, MD, PhD
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Clinical Fellow
Biography
Shan Parikh, MD, PhD, is a cardiologist based in New Haven, Connecticut, specializing in preventive cardiology, lipid disorders, and cardiometabolic disease. He completed his Internal Medicine residency and Cardiovascular Disease fellowship at Yale New Haven Hospital and earned his MD and PhD from Vanderbilt University School of Medicine. Dr. Parikh is also an active physician-scientist whose research focuses on myocardial metabolism, insulin resistance, and cardiovascular disease, with publications in leading journals including Circulation and Circulation Research. He believes that the best cardiovascular care combines evidence-based medicine with a personalized understanding of each patient's goals, values, and unique health risks. His goal is to help patients prevent heart disease, optimize long-term health, and make informed decisions through collaborative, compassionate care. As both a clinician and researcher, he remains committed to translating scientific advances into practical strategies that improve cardiovascular health and quality of life.
Last Updated on August 03, 2026.
Departments & Organizations
Education & Training
- Resident
- Yale University (2022)
- MD
- Vanderbilt University School of Medicine (2020)
- PhD
- Vanderbilt University, Pharmacology (2018)
- MS
- University of Connecticut, Physiology and Neurobiology (2011)
- BS
- University of Connecticut , Physiology and Neurobiology (2010)
Board Certifications
Internal Medicine
- Certification Organization
- AB of Internal Medicine
- Original Certification Date
- 2023
Research
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Overview
Medical Research Interests
Cardiovascular Abnormalities; Cardiovascular Diseases; Fatty Liver; Glucose Metabolism Disorders; Heart Diseases; Heart Failure; Vascular Diseases
Public Health Interests
Aging; Cardiovascular Diseases; Metabolism; Obesity
ORCID
0000-0003-1806-9199
Research at a Glance
Publications Timeline
A big-picture view of Shan S. Parikh's research output by year.
11Publications
1,028Citations
Publications
Featured Publications
Impaired Dynamic Sarcoplasmic Reticulum Ca Buffering in Autosomal Dominant CPVT2
Wleklinski M, Kryshtal D, Kim K, Parikh S, Blackwell D, Marty I, Iyer V, Knollmann B. Impaired Dynamic Sarcoplasmic Reticulum Ca Buffering in Autosomal Dominant CPVT2. Circulation Research 2022, 131: 673-686. PMID: 36102198, PMCID: PMC9529867, DOI: 10.1161/circresaha.121.320661.Peer-Reviewed Original ResearchCitationsAltmetricPatient-independent human induced pluripotent stem cell model: A new tool for rapid determination of genetic variant pathogenicity in long QT syndrome
Chavali NV, Kryshtal DO, Parikh SS, Wang L, Glazer AM, Blackwell DJ, Kroncke BM, Shoemaker MB, Knollmann BC. Patient-independent human induced pluripotent stem cell model: A new tool for rapid determination of genetic variant pathogenicity in long QT syndrome. Heart Rhythm 2019, 16: 1686-1695. PMID: 31004778, PMCID: PMC6935564, DOI: 10.1016/j.hrthm.2019.04.031.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLong QT syndromeExtracellular field potentialsQT syndromeHiPSC-CMGenetic testingPluripotent stem cell modelsHiPSC modelsSudden cardiac deathStem cell modelUnrelated healthy volunteersVentricular action potentialPatch-clamp studiesNovel missense variantVoltage-dependent inactivationCardiac deathClinical benefitCommercial genetic testingGenetic variant pathogenicityHealthy volunteersCell modelElectrophysiological propertiesAction potentialsBeating rateUnknown significancePatch clampThyroid and Glucocorticoid Hormones Promote Functional T-Tubule Development in Human-Induced Pluripotent Stem Cell–Derived Cardiomyocytes
Parikh SS, Blackwell DJ, Gomez-Hurtado N, Frisk M, Wang L, Kim K, Dahl CP, Fiane A, Tønnessen T, Kryshtal DO, Louch WE, Knollmann BC. Thyroid and Glucocorticoid Hormones Promote Functional T-Tubule Development in Human-Induced Pluripotent Stem Cell–Derived Cardiomyocytes. Circulation Research 2017, 121: 1323-1330. PMID: 28974554, PMCID: PMC5722667, DOI: 10.1161/circresaha.117.311920.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHuman-induced pluripotent stem cell-derived cardiomyocytesExcitation-contraction couplingPluripotent stem cell-derived cardiomyocytesCa releaseGlucocorticoid hormonesStem cell-derived cardiomyocytesCell-derived cardiomyocytesCa-induced Ca releaseT-tubule developmentAdult human ventricular cardiomyocytesExtensive T-tubule networkHuman ventricular cardiomyocytesL-type Ca channelsL-type CaT-tubulesIntracellular Ca releaseCell-based therapiesConfocal line scanHeart diseaseT-tubule networkFunctional maturationVentricular cardiomyocytesPermissive roleDay 16Ca channels
2023
Regulation of Postnatal Cardiomyocyte Maturation by an RNA Splicing Regulator RBFox1
Huang J, Lee J, Rau C, Pezhouman A, Yokota T, Miwa H, Feldman M, Kong T, Yang Z, Tay W, Pushkarsky I, Kim K, Parikh S, Udani S, Soh B, Gao C, Stiles L, Shirihai O, Knollmann B, Ardehali R, Di Carlo D, Wang Y. Regulation of Postnatal Cardiomyocyte Maturation by an RNA Splicing Regulator RBFox1. Circulation 2023, 148: 1263-1266. PMID: 37844148, PMCID: PMC10593507, DOI: 10.1161/circulationaha.122.061602.Peer-Reviewed Original ResearchCitationsAltmetric
2022
Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization
Bersell K, Yang T, Mosley J, Glazer A, Hale A, Kryshtal D, Kim K, Steimle J, Brown J, Salem J, Campbell C, Hong C, Wells Q, Johnson A, Short L, Blair M, Behr E, Petropoulou E, Jamshidi Y, Benson M, Keyes M, Ngo D, Vasan R, Yang Q, Gerszten R, Shaffer C, Parikh S, Sheng Q, Kannankeril P, Moskowitz I, York J, Wang T, Knollmann B, Roden D. Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization. Circulation 2022, 147: 824-840. PMID: 36524479, PMCID: PMC9992308, DOI: 10.1161/circulationaha.122.062193.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPlatelet-derived growth factorInduced pluripotent stem cellsBrugada syndromeArrhythmia syndromesSerum platelet-derived growth factorSodium currentGeneral transcriptional mechanismFramingham Heart Study cohortPI3KPDGF receptor expressionLate sodium currentCardiac sodium currentCardiac transcription factorsSmall molecule perturbationsCurrent-clamp experimentsCardiac sodium channel geneSodium channel geneFramingham Heart StudyMurine model systemPluripotent stem cellsMonogenic arrhythmia syndromesReceptor blockadeElectrophysiologic abnormalitiesQTc intervalStudy cohort
2018
Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model
Gupte M, Tumuluru S, Sui JY, Singh AP, Umbarkar P, Parikh SS, Ahmad F, Zhang Q, Force T, Lal H. Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model. International Journal Of Cardiology 2018, 259: 145-152. PMID: 29398139, PMCID: PMC5869114, DOI: 10.1016/j.ijcard.2018.01.013.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHigh-fat dietAdverse ventricular remodelingCardiac dysfunctionCardiac functionVentricular remodelingBody weightGSK-3βControl dietHeart weight/tibia lengthDiet-induced cardiac dysfunctionIndependent risk factorImpaired cardiac functionSevere cardiac dysfunctionFat mass compositionLittermate control miceProtective compensatory mechanismCardiomyocyte-specific deletionComparable body weightTibia lengthTransthoracic echocardiographyControl miceObesity modelRisk factorsMyocardial diseaseDysfunction
2017
Hypertrophic cardiomyopathy-linked mutation in troponin T causes myofibrillar disarray and pro-arrhythmic action potential changes in human iPSC cardiomyocytes
Wang L, Kim K, Parikh S, Cadar AG, Bersell KR, He H, Pinto JR, Kryshtal DO, Knollmann BC. Hypertrophic cardiomyopathy-linked mutation in troponin T causes myofibrillar disarray and pro-arrhythmic action potential changes in human iPSC cardiomyocytes. Journal Of Molecular And Cellular Cardiology 2017, 114: 320-327. PMID: 29217433, PMCID: PMC5800960, DOI: 10.1016/j.yjmcc.2017.12.002.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMyofilament Ca sensitivityHiPSC-CMsControl hiPSC-CMsCa handlingTroponin TAction potentialsAction potential triangulationPro-arrhythmic changesCa sensitivityHuman ventricular action potentialCardiac troponin TAction potential changesIntracellular Ca transientsVentricular action potentialHuman iPSC-cardiomyocytesRod-shaped cardiomyocytesCardiac action potentialDiastolic dysfunctionImpaired relaxationSystolic functionVentricular arrhythmiasHypertrophic cardiomyopathySudden deathArrhythmia riskCardiac hypertrophyMyofilament Calcium-Buffering Dependent Action Potential Triangulation in Human-Induced Pluripotent Stem Cell Model of Hypertrophic Cardiomyopathy
Wang L, Kryshtal DO, Kim K, Parikh S, Cadar AG, Bersell KR, He H, Pinto JR, Knollmann BC. Myofilament Calcium-Buffering Dependent Action Potential Triangulation in Human-Induced Pluripotent Stem Cell Model of Hypertrophic Cardiomyopathy. Journal Of The American College Of Cardiology 2017, 70: 2600-2602. PMID: 29145956, PMCID: PMC5805484, DOI: 10.1016/j.jacc.2017.09.033.Commentaries, Editorials and LettersCitationsAltmetricFrequency of mononuclear diploid cardiomyocytes underlies natural variation in heart regeneration
Patterson M, Barske L, Van Handel B, Rau CD, Gan P, Sharma A, Parikh S, Denholtz M, Huang Y, Yamaguchi Y, Shen H, Allayee H, Crump JG, Force TI, Lien CL, Makita T, Lusis AJ, Kumar SR, Sucov HM. Frequency of mononuclear diploid cardiomyocytes underlies natural variation in heart regeneration. Nature Genetics 2017, 49: 1346-1353. PMID: 28783163, PMCID: PMC5736145, DOI: 10.1038/ng.3929.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAnimals, Genetically ModifiedCells, CulturedDiploidyGene Expression ProfilingHeartImmunoblottingIn Situ Hybridization, FluorescenceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, ConfocalMyocardiumMyocytes, CardiacProtein KinasesProtein Serine-Threonine KinasesRegenerationZebrafish
2016
Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy
Zhou J, Ahmad F, Parikh S, Hoffman NE, Rajan S, Verma VK, Song J, Yuan A, Shanmughapriya S, Guo Y, Gao E, Koch W, Woodgett JR, Madesh M, Kishore R, Lal H, Force T. Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy. Circulation Research 2016, 118: 1208-1222. PMID: 26976650, PMCID: PMC4843504, DOI: 10.1161/circresaha.116.308544.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAdult cardiac myocytesCardiac myocytesCardiac homeostasisGSK-3βSerial echocardiographic analysisCardiac myocyte-specific deletionGSK-3Normal cardiac homeostasisMitotic catastropheCell cycle dysregulationDouble knockout heartsVentricular dysfunctionOverall survivalTamoxifen treatmentCardiac protectionMyocardial infarctionEchocardiographic analysisHeart functionGlycogen synthase kinaseIsolated adult cardiac myocytesSynergistic protectionGSK-3 isoformsCell cycle activityMarked activationCell cycle progression
Clinical Trials
Current Trials
DAL-302
IRB ID2000039690RoleSub InvestigatorPrimary Completion Date08/31/2027Recruiting ParticipantsGenderBothAge45+ years
Academic Achievements & Community Involvement
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activity TLC-1180 Reverses Obesity, Improves Myocardial Insulin Sensitivity, and Enhances Cardiac Fitness in a Murine Model of Diet-Induced Obesity
01/29/2026 - PresentOral PresentationCardiometabolism in Health and Disease, Keystone SymposiumDetailsKeystone, CO, United States
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The Anlyan Center
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300 Cedar Street
New Haven, CT 06519
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