Physician
Cardiology
Dr. Jonathan C. Makielski, MD
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Doctor Jonathan C. Makielski, MD is an expert in the field of Cardiology. He studied medicine at University of Chicago Pritzker School of Medicine. University of Chicago Pritzker School of Medicine is ranked 10/19 in Research/PrimaryCare. He received 1 awards: "Meaningful Use Stage 1 Certification". Jonathan Makielski is a published physician as well. He has 101 publications published. The latest was: Post-repolarization block of cardiac sodium channels by saxitoxin. He accepts Medicare payments and is registered with Medicare.gov.
Publications
- Identification of rare variants of DSP gene in sudden unexplained nocturnal death Syndrome in the southern Chinese Han population.
- In memoriam: harry a. Fozzard, MD, april 22, 1931-december 9, 2014.
- Mouse ERG K(+) channel clones reveal differences in protein trafficking and function.
- Diseases caused by mutations in Nav1.5 interacting proteins.
- Calcium Transients Closely Reflect Prolonged Action Potentials in iPSC Models of Inherited Cardiac Arrhythmia.
- Abcc9 is required for the transition to oxidative metabolism in the newborn Heart.
- KCNJ2 Mutation Causes an Adrenergic-Dependent Rectification Abnormality with Calcium Sensitivity and Ventricular Arrhythmia.
- ATP-sensitive potassium currents from channels formed by Kir6 and a modified cardiac mitochondrial SUR2 variant.
- The Interaction of Caveolin 3 with the Inward Rectifier Channel Kir2.1; Physiology and Pathology related to LQT9.
- Channelopathies from mutations in the cardiac sodium channel protein complex.
- Caveolin-3 suppresses late sodium current by inhibiting nNOS-dependent S-nitrosylation of SCN5A.
- Redox Control of Cardiac Excitability.
- Loss-of-Function Mutations in the KCNJ8-Encoded Kir6.1 KATP Channel and Sudden Infant Death Syndrome.
- The common African American polymorphism SCN5A-S1103Y interacts with mutation SCN5A-R680H to increase late Na current.
- The mitochondrial bioenergetic phenotype for protection from cardiac ischemia in SUR2 mutant mice.
- SCN5A rare variants in familial dilated Cardiomyopathy decrease peak sodium current depending on the common polymorphism H558R and common splice variant Q1077del.
- Cardiomyocyte sulfonylurea receptor 2-KATP channel mediates cardioprotection and ST segment elevation.
- Gain-of-function mutation S422L in the KCNJ8-encoded cardiac K(ATP) channel Kir6.1 as a pathogenic substrate for J-wave Syndromes.
- Epidemiologic, molecular, and functional evidence suggest A572D-SCN5A should not be considered an independent LQT3-susceptibility mutation.
- Sudden infant death Syndrome-associated mutations in the sodium channel beta subunits.
- Sudden Unexplained Nocturnal Death Syndrome in Southern China: An Epidemiological Survey and SCN5A Gene Screening.
- Alpha1-syntrophin mutations identified in sudden infant death Syndrome cause an increase in late cardiac sodium current.
- Molecular identification and functional characterization of a mitochondrial sulfonylurea receptor 2 splice variant generated by intraexonic splicing.
- Use-dependent block of cardiac late Na(+) current by ranolazine.
- GPD1L links redox state to cardiac excitability by PKC-dependent phosphorylation of the sodium channel SCN5A.
- Protein kinase A-dependent biophysical phenotype for V227F-KCNJ2 mutation in catecholaminergic polymorphic ventricular tachycardia.
- Unique mixed phenotype and unexpected functional effect revealed by novel compound heterozygosity mutations involving SCN5A.
- Sodium channel mutation in irritable bowel Syndrome: evidence for an ion channelopathy.
- Syntrophin mutation associated with long QT Syndrome through activation of the nNOS-SCN5A macromolecular complex.
- A mutation in telethonin alters Nav1.5 function.
- Suppression of atrial fibrillation with mexiletine pharmacotherapy in a young woman with type 1 long QT Syndrome.
- Inherited arrhythmias: a National Heart, Lung, and Blood Institute and Office of Rare Diseases workshop consensus report about the diagnosis, phenotyping, molecular me...
- Molecular and functional characterization of novel glycerol-3-phosphate dehydrogenase 1 like gene (GPD1-L) mutations in sudden infant death Syndrome.
- SCN4B-encoded sodium channel beta4 subunit in congenital long-QT Syndrome.
- KCNJ2 mutations in arrhythmia patients referred for LQT testing: a mutation T305A with novel effect on rectification properties.
- Novel mechanism for sudden infant death Syndrome: persistent late sodium current secondary to mutations in caveolin-3.
- Mutant caveolin-3 induces persistent late sodium current and is associated with long-QT Syndrome.
- Partial expression Defect for the SCN5A missense mutation G1406R depends on splice variant background Q1077 and rescue by mexiletine.
- Genotypic heterogeneity and phenotypic mimicry among unrelated patients referred for catecholaminergic polymorphic ventricular tachycardia genetic testing.
- Na(+) current in human ventricle: implications for sodium loading and homeostasis.
- Spontaneous Coronary vasospasm in KATP mutant mice arises from a smooth muscle-extrinsic process.
- Specific serine proteases selectively damage KCNH2 (hERG1) potassium channels and I(Kr).
- SIDS: genetic and environmental influences may cause arrhythmia in this silent killer.
- Common human SCN5A polymorphisms have altered electrophysiology when expressed in Q1077 splice variants.
- The perplexing complexity of cardiac Arrhythmias: beyond electrical remodeling.
- Spectrum and prevalence of cardiac sodium channel variants among black, white, Asian, and Hispanic individuals: implications for arrhythmogenic susceptibility and Brug...
- Targeted mutational analysis of the RyR2-encoded cardiac ryanodine receptor in sudden unexplained death: a molecular autopsy of 49 medical examiner/coroner's cases.
- A ubiquitous splice variant and a common polymorphism affect heterologous expression of recombinant human SCN5A Heart sodium channels.
- A common human SCN5A polymorphism modifies expression of an arrhythmia causing mutation.
- Genetic basis for the origin of cardiac Arrhythmias: implications for therapy.
- Episodic Coronary artery vasospasm and hypertension develop in the absence of Sur2 K(ATP) channels.
- Loss-of-function mutation of the SCN3B-encoded sodium channel {beta}3 subunit associated with a case of idiopathic ventricular Fibrillation.
- Fatty acids antagonize bupivacaine-induced I(Na) blockade.
- Differential modulation of late sodium current by protein kinase A in R1623Q mutant of LQT3.
- Cardiac sulfonylurea receptor short form-based channels confer a glibenclamide-insensitive KATP activity.
- Rate-dependent QT shortening mechanism for the LQT3 deltaKPQ mutant.
- The single nucleotide polymorphisms of I(Ks) potassium channel genes and their association with Atrial fibrillation in a Chinese population.
- Mice lacking sulfonylurea receptor 2 (SUR2) ATP-sensitive potassium channels are resistant to Acute cardiovascular stress.
- A novel C-terminal truncation SCN5A mutation from a patient with sick sinus Syndrome, conduction disorder and ventricular tachycardia.
- Ranolazine and late cardiac sodium current--a therapeutic target for Angina, arrhythmia and more?
- Function and distribution of the SUR isoforms and splice variants.
- A trafficking defective, Brugada Syndrome-causing SCN5A mutation rescued by drugs.
- Intrinsic mechanism of the enhanced rate-dependent QT shortening in the R1623Q mutant of the LQT3 Syndrome.
- Increased late sodium current in myocytes from a canine Heart failure model and from failing human Heart.
- Blockade of HERG cardiac K+ current by antifungal drug miconazole.
- Arrhythmia mutations in non-coding region of SCN5A: implications for genetic screening.
- Late Na currents affected by alpha subunit isoform and beta1 subunit co-expression in HEK293 cells.
- A novel SCN5A arrhythmia mutation, M1766L, with expression Defect rescued by mexiletine.
- Syntrophin gamma 2 regulates SCN5A gating by a PDZ domain-mediated interaction.
- Drug-induced long QT Syndrome: hERG K+ channel block and disruption of protein trafficking by fluoxetine and norfluoxetine.
- Transient left ventricular apical ballooning: a review of the literature.
- Inward sodium current at resting potentials in single cardiac myocytes induced by the ischemic metabolite lysophosphatidylcholine.
- Modulation of cardiac sodium channel gating by lysophosphatidylcholine.
- External site for local anesthetic block of cardiac Na+ channels.
- Two components of use-dependent block of sodium current by lidocaine in voltage clamped cardiac Purkinje cells.
- Triggered activity in the Heart: cellular mechanisms of early after-depolarizations.
- Block of sodium current by heptanol in voltage-clamped canine cardiac Purkinje cells.
- Temperature dependence of sodium current block by lidocaine in cardiac Purkinje cells.
- Modulating intraventricular conduction through competition of two class 1 antiarrhythmic agents: experience with ethacizin and lidocaine in canine Heart.
- State dependence of ethacizin and ethmozin block of sodium current in voltage clamped and internally perfused cardiac Purkinje cells.
- Comments on "Effect of cellular uncoupling by heptanol on conduction in infarcted myocardium".
- Quinidine blocks adenosine 5'-triphosphate-sensitive potassium channels in Heart.
- Sodium currents in single cardiac Purkinje cells.
- Open sodium channel properties of single canine cardiac Purkinje cells.
- Effect of prolonged depolarizations on twitch tension and intracellular sodium activity in sheep cardiac Purkinje fibres.
- Sodium channels in cardiac Purkinje cells.
- Use-dependent block of sodium current by ethmozin in voltage-clamped internally perfused canine cardiac Purkinje cells.
- Single channel sodium current in rat cardiomyocytes: use-dependent block by ethacizin.
- Is there a second external lidocaine binding site on mammalian cardiac cells?
- New studies of the excitatory sodium currents in Heart muscle.
- The electrophysiology of Acute myocardial ischemia.
- Sodium current in voltage clamped internally perfused canine cardiac Purkinje cells.
- Combination ethacizin and ethmozin treatment of resistant ventricular ectopy: theoretical, experimental, and clinical study.
- Cytoskeleton modulates gating of voltage-dependent sodium channel in Heart.
- Modulation of ATP-sensitive K+ channels by internal acidification in insulin-secreting cells.
- ATP-sensitive K+ channel opener acts as a potent Cl- channel inhibitor in vascular smooth muscle cells.
- Post-repolarization block of cloned sodium channels by saxitoxin: the contribution of pore-region amino acids.
- Cytoplasmic acidosis induces multiple conductance states in ATP-sensitive potassium channels of cardiac myocytes.
- Kinetic effects of quaternary lidocaine block of cardiac sodium channels: a gating current study.
- Post-repolarization block of cardiac sodium channels by saxitoxin.
Schools
University Of ChicagoThe Pritzker School Of Medicine
North Carolina Memorial Hospital
University of Chicago
Procedures Preformed
- Cardiac Catheterization (incl. Coronary Angiography)
- Cardiac Imaging
- Cardiac Myocardial Perfusion Imaging
- Cardioverter-Defibrillator or Pacemaker Insertion, Removal or Repair
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Conditions Treated
- Aneurysm and Dissection of Heart
- Angina and Acute Coronary Syndrome
- Aortic Aneurysm
- Aortic Valve Disease
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Doctors Specialties
- Cardiology
Accepted Insurances
Awards
- Meaningful Use Stage 1 Certification
Education
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University of Chicago -
University of North Carolina Hospitals -
University of Chicago Pritzker School of Medicine
Hospital
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University of Wisconsin Hospital and Clinics -
William S. Middleton Memorial Veterans Hospital
Drug Facts
| NPI NUMBER | 1255308193 | |
| NPPES Provider LastName | MAKIELSKI | |
| NPPES Provider FirstName | JONATHAN | |
| NPPES Provider ZIPCode | 537920001 | |
| NPPES Provider State | WI | |
| Specialty Description | Cardiology | |
| Total Claim Count | 61.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1255308193 |
| Last Name Of The Provider | MAKIELSKI |
| First Name Of The Provider | JONATHAN |
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