A message from Dr. Maria I. Kontaridis, Ph.D, Executive Director, Director of Research, Gordon K. Moe Professor and Chair of Biomedical Research and Translational Medicine.
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To trace the first 50 years of the Laboratory’s work is to follow a timeline of profound scientific achievement and impact.
Research support contributes to the defeat of rheumatic fever, the leading cause of death in young children.
Gerontology program is established.
Experimental Cardiology program initiated to study heart disease.
Neurophysiology program begins with a focus on vision research.
Summer Fellowship and Predoctoral and Postdoctoral programs begin.
Several mechanisms of cardiac arrhythmia are defined and characterized including those responsible for AV nodal tachycardia, atrial fibrillation and atrial flutter. Discovery of dual AV nodal pathways lays the foundation for subsequent treatment and cure of AV nodal tachycardias using radio frequency ablation.
The mechanism by which Digitalis produces dangerous arrhythmias is uncovered.
Cancer program is established.
Blood substitute program is established.
The vision program demonstrates how light entering the eye generates neural activity responsible for recognition of objects.
Muscular dystrophy research commences.
The role of free oxygen radicals in aging and disease becomes a major focus of study.
Hypertension researchers investigate actions of beta blockers like Inderal.
Life extension is demonstrated by restriction of caloric intake.
Vitamin A is shown to play a vital role in preventing cancer.
Accumulation of metal ions in the body as a function of age is shown to decrease lifespan and contribute to disease.
Modulated parasystole is discovered as a mechanism of cardiac arrhythmia.
Reflection is discovered as a mechanism of cardiac arrhythmia.
Mechanisms of action of several cardioactive drugs are defined (Quinidine, Propranolol, Digitalis, Lidocaine, Procainamide, Amiloride, Amrinone, Milrinone, Sotalol, and Amiodarone).
A link between cancer and atherosclerosis is found.
Differences in the electrical activity of the inside versus the outside muscle of the heart are discovered and shown to contribute to differential responsiveness to drugs.
Benzo(a)pyrene, a common environmental pollutant and a carcinogenic component of cigarette smoke, is shown to contribute to hardening of the arteries, as well as to produce other harmful health effects.
Aging research finds that mitochondrial DNA breaks down with aging, and that aluminum and iron ions can increase the rate of aging.
The cancer program studies Adriamycin, a drug used in cancer chemotherapy.
The gerontology program assesses the role of vitamin C in aging.
The gerontology program studies the bone loss that occurs during normal aging, suggesting that excess iron may contribute to osteoporosis.
A blood substitute is developed and patented.
A new cell type, the M cell, is discovered in the heart.
Immunology program is established.
The immune system is implicated in the development of essential hypertension.
Electrical heterogeneity in the heart becomes a major focus of the Experimental Cardiology program. The immunology program initiates research into autoimmune diseases such as lupus and rheumatoid arthritis. The Laboratory is granted a patent for the treatment of lupus erythematosus.
Scientists link erythromycin — in rare cases — to sudden cardiac death. Phase 2 re-entry is discovered as a mechanism of cardiac arrhythmia linked to tachycardia and sudden death.
Molecular Biology program is established.
Mid cells are shown to be more sensitive to many drugs that affect the heart.
Mid cells are linked to pathophysiological T waves in ECG.
The long QT syndrome, a hereditary affliction that can result in sudden death, is studied. Experimental models of long QT syndrome are developed and drugs effective in suppressing arrhythmias caused by this condition are identified.
The first gene responsible for sudden cardiac death is discovered. The basis of the J wave and T wave of the ECG is uncovered.
Mechanisms responsible for the life-threatening long QT and Brugada syndromes are proposed. Drug treatment is established for people with a high risk for sudden cardiac death from Brugada syndrome.
Experimental models of Brugada syndrome, and inherited cardiac sudden death syndrome, are developed.
A genetic basis for Brugada syndrome is discovered.
The Molecular Genetics program is established.
The Laboratory begins research on human heart tissue in collaboration with the Mohawk Valley Heart Institute.
The Laboratory begins to study sudden infant death syndrome and discovers direct evidence linking SIDS to an abnormal heart rhythm.
MMRL scientists delineate the mechanism responsible for sudden death in children afflicted with an inherited syndrome called catecholaminergic polymorphic ventricular tachycardia (CPVT), which causes sudden death when they exercise vigorously.
A genetic basis for short QT syndrome is discovered, linking the syndrome to an ion channel defect in the heart, and quinidine is identified as an effective adjunct treatment drug.
A study designed to examine the contribution of genetic mutations to arrhythmogenesis in a cohort of patients who developed one or more episodes of ventricular tachycardia and fibrillation during acute myocardial infarction is conducted, resulting in the identification of a gene mutation.
A cardiac gene in nerve cells located in the fat pads of the heart is identified, a finding with broad implications for understanding a number of inherited diseases associated with cardiac sodium channel mutations.
Scientists identify a polymorphism in the potassium channel (K897T) that appears to contribute to ventricular tachycardia after a heart attack.
A Laboratory study suggests a new strategy for the treatment of atrial fibrillation using atrial-selective sodium channel blockers such as ranolazine
In 2003, the MMRL established a Stem Cell Center to leverage the power of induced pluripotent stem cell technology in the study of cardiac arrhythmias.
Discovered that a combination of ranolazine (Ranexa) and dronedarone (Multaq) creates a synergistic effect on the upper chambers of the heart resulting in suppression of atrial fibrillation. A phase 2 clinical trial, named HARMONY, was initiated by Gilead Sciences on the basis of these findings.
Phase 2 Clinical Trial of the new drug combination are successful and plans for Phase 3 Clinical Trial are under development by Gilead Sciences.
The Molecular Genetics Program gained several new tools to detect and identify gene mutations that cause inherited cardiac arrhythmias. Next generation sequencing was implemented . The Ion Torrent sequencer was funded in part by a grant from the New York State Regional Economic Development Council.
The MMRL was selected to receive a $1,750,000 grant award from the National Institutes of Health in 2010 as well as a $1,080,000 grant from the New York State Stem Cell Science.
A study published in Circulation Cardiovascular Genetics, a Journal of the American Heart Association identified a specific gene mutation that can lead to Sudden Infant Death Syndrome. An MMRL study published in the Journal of the American College of Cardiology demonstrates that simvastatin may have a beneficial effect in patients afflicted with certain types of cardiac arrhythmias.
In 2012, the MMRL inaugurated Organ and Tissue Bioengineering Program focused on building new hearts for transplantation in individuals with end-stage heart failure and other forms of heart disease.
A temporal window of vulnerability to atrial fibrillation during heart failure was discovered.
In 2014, the Laboratory identified a gene labeled SCN10A as a cause of cardiac arrhythmias. Previously, this gene was thought to only effect sodium channels in the brain.