Vanderbilt University School of Medicine

Internal Medicine

Doctor Bjoern C. Knollmann, MD is an expert in the field of Internal Medicine. He went to medical school at University of Cincinnati College of Medicine. He received awards:"Elected Member". Bjoern C. Knollmann is a published MD as well. He has 49 publications published. The latest was: Cardiac actions of erythromycin: influence of female sex.

Publications

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• Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVT.
• In Vitro Studies Indicate Intravenous Lipid Emulsion Acts as Lipid Sink in Verapamil Poisoning.
• Modelling sarcomeric cardiomyopathies in the dish: from human heart samples to iPSC cardiomyocytes.
• Impaired calcium-calmodulin-dependent inactivation of Cav1.2 contributes to loss of sarcoplasmic reticulum calcium release refractoriness in mice lacking calsequestrin 2.
• Sinus node dysfunction in catecholaminergic polymorphic ventricular tachycardia: Risk factor and potential therapeutic target?
• Screening for Acute IKr Block is Insufficient to Detect Torsades de Pointes Liability: Role of Late Sodium Current.
• Myofilament ca sensitization increases cytosolic ca binding affinity, alters intracellular ca homeostasis, and causes pause-dependent ca-triggered arrhythmia.
• Suppression of Spontaneous Ca Elevations Prevents Atrial Fibrillation in Casq2 Null Hearts.
• Carvedilol tweaks calcium release to ease arrhythmias.
• Inositol 1,4,5-trisphosphate receptors: "exciting" players in cardiac excitation-contraction coupling?
• Myofilament calcium de-sensitization and contractile uncoupling prevent pause-triggered ventricular tachycardia in mouse hearts with chronic myocardial infarction.
• Induced pluripotent stem cell-derived cardiomyocytes: boutique science or valuable arrhythmia model?
• Parameter Sensitivity Analysis of Stochastic Models Provides Insights into Cardiac Calcium Sparks.
• Triadin regulates cardiac muscle couplon structure and microdomain Ca2+ signalling: a path towards ventricular arrhythmias.
• Flecainide therapy reduces exercise-induced ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia.
• Accelerated sinus rhythm prevents catecholaminergic polymorphic ventricular tachycardia in mice and in patients.
• Coordinated Regulation of Murine Cardiomyocyte Contractility by Nanomolar (-)-epigallocatechin-3-gallate, the Major Green Tea Catechin.
• Accelerated Junctional Rhythm and Nonalternans Repolarization Lability Precede Ventricular Tachycardia in Casq2-/- Mice.
• Calsequestrin mutations and catecholaminergic polymorphic ventricular tachycardia.
• Ryanodine receptor inhibition potentiates the activity of Na channel blockers against spontaneous calcium elevations and delayed afterdepolarizations in Langendorff-pe...
• Calsequestrin 2 and arrhythmias.
• Efficacy and potency of class I antiarrhythmic drugs for suppression of Ca2+ waves in permeabilized myocytes lacking calsequestrin.
• Mechanism of antiarrhythmic effects of flecainide in catecholaminergic polymorphic ventricular tachycardia.
• Striking In Vivo Phenotype of a Disease-Associated Human SCN5A Mutation Producing Minimal Changes in Vitro.
• Oxidized CaMKII: a "heart stopper" for the sinus node?
• Gauging the risk of arrhythmic death by common genetic variants: resurgence of the sinister QT.
• Inhibition of cardiac Ca2+ release channels (RyR2) determines efficacy of class I antiarrhythmic drugs in catecholaminergic polymorphic ventricular tachycardia.
• Genetics of sudden cardiac death syndromes.
• Flecainide inhibits arrhythmogenic Ca2+ waves by open state block of ryanodine receptor Ca2+ release channels and reduction of Ca2+ spark mass.
• New roles of calsequestrin and triadin in cardiac muscle.
• Ablation of triadin causes loss of cardiac Ca2+ release units, impaired excitation-contraction coupling, and cardiac arrhythmias.
• Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans.
• Amitriptyline activates cardiac ryanodine channels and causes spontaneous sarcoplasmic reticulum calcium release.
• Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca2+ release, and catecholaminergic polymorphic ventricular tachycardia.
• Altered regulation of cardiac muscle contraction by troponin T mutations that cause familial hypertrophic cardiomyopathy.
• Assessment of joint review of radiologic studies by a primary care physician and a radiologist.
• Cardiac actions of erythromycin: influence of female sex.
• Inotropic stimulation induces cardiac dysfunction in transgenic mice expressing a troponin T (I79N) mutation linked to familial hypertrophic cardiomyopathy.
• Targeted disruption of the Kcnq1 gene produces a mouse model of Jervell and Lange-Nielsen Syndrome.
• Remodelling of ionic currents in hypertrophied and failing hearts of transgenic mice overexpressing calsequestrin.
• Monophasic action potential recordings from intact mouse heart: validation, regional heterogeneity, and relation to refractoriness.
• Calsequestrin 2 deletion shortens the refractoriness of Ca²⁺ release and reduces rate-dependent Ca²⁺-alternans in intact mouse hearts.
• Quantification of calsequestrin 2 (CSQ2) in sheep cardiac muscle and Ca2+-binding protein changes in CSQ2 knockout mice.
• Paradoxical buffering of calcium by calsequestrin demonstrated for the calcium store of skeletal muscle.
• A "rough" journey to the sarcoplasmic reticulum--implications of altered calsequestrin trafficking for cardiac arrhythmia.
• Kcnq1 contributes to an adrenergic-sensitive steady-state K+ current in mouse heart.
• Recombinase-mediated cassette exchange to rapidly and efficiently generate mice with human cardiac sodium channels.
• Isoproterenol exacerbates a long QT phenotype in Kcnq1-deficient neonatal mice: possible roles for human-like Kcnq1 isoform 1 and slow delayed rectifier K+ current.

Schools

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• University of Cincinnati Main Campus

• Georgetown University Mc

Doctors Specialties

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• Internal Medicine

Accepted Insurances

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Awards

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• Elected Member

Education

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• Georgetown University Hospital
• University of Cincinnati College of Medicine

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