• sudden cardi
  • He undertook residency training in anesthesiology and fellowship training in cardiac anesthesiology and in critical care medicine at The Johns Hopkins Hospital in Baltimore, MD. He joined the faculty at Johns Hopkins in 1995, where he practiced cardiac anesthesiology, ICU medicine, and led an NIH-funded research program aimed at the genetics of cardiac rhythm disorders, such as sudden cardiac death. (wikipedia.org)
  • contractility
  • Their effect on cardiac contractility has not been assessed directly. (ahajournals.org)
  • Conclusions- Pantoprazole depresses cardiac contractility in vitro by depression of Ca 2+ signaling and myofilament activity. (ahajournals.org)
  • Ca 2+ influx through the L-type Ca 2+ channel ( I Ca,L ) is a key determinant of cardiac contractility and is modulated by multiple signaling pathways. (ahajournals.org)
  • Similarly, gain of function of Na+ and Ca2+ channels results in delayed repolarization, and Ca2+ overload causing increased Ca2+ binding to cardiac troponin C, more actin-myosin interactions and causing an increased contractility, respectively. (wikipedia.org)
  • The short- and long-term use of this therapy enhances the strength of ventricular contraction and therefore the heart's pumping capacity by modulating (adjusting) the myocardial contractility. (wikipedia.org)
  • The Cardiac contractility modulation treatment is delivered by a pacemaker-like device that applies non-excitatory electrical signals NES, adjusted to and synchronized with the electrical action in the cardiac cycle. (wikipedia.org)
  • Other than a pacemaker, which delivers an electrical signal with the intention to result in cardiac contraction, the Cardiac contractility modulation treatment applies the NES, adjusted to and synchronized with the electrical action in the cardiac cycle. (wikipedia.org)
  • In Cardiac contractility modulation therapy, electrical stimulation is applied to the cardiac muscle during the absolute refractory period. (wikipedia.org)
  • In contrast to other electrical stimulation treatments for heart failure, such as pacemaker therapy or implantable cardioverter defibrillators (ICD), Cardiac contractility modulation does not affect the cardiac rhythm directly. (wikipedia.org)
  • Rather, the aim is to enhance the heart's natural contraction (the native cardiac contractility) sustainably over long periods of time. (wikipedia.org)
  • Furthermore, unlike most interventions that increase cardiac contractility, the Cardiac contractility modulation is not associated with an unfavorable increase in oxygen demand by the heart (measured in terms of Myocardial Oxygen Consumption or MVO2). (wikipedia.org)
  • A meta-analysis in 2014 and an overview of device-based treatment options in heart failure in 2013 concluded that Cardiac contractility modulation treatment is safe, that it is generally beneficial to patients and that the treatment increases the exercise tolerance (ET) and quality of life (QoL) of patients. (wikipedia.org)
  • Furthermore, preliminary long-term survival data shows that Cardiac contractility modulation is associated with lower long-term mortality in heart failure patients when compared with expected rates among similar patients not treated with Cardiac contractility modulation. (wikipedia.org)
  • Based on the results of clinical trials, Cardiac contractility modulation devices are approved and available for clinical use in all European Union countries and in Australia, Turkey, India and Hong Kong, as well as in other countries that recognize CE marking for medical devices. (wikipedia.org)
  • At the present time, Cardiac contractility modulation therapy is not approved for clinical use in the United States. (wikipedia.org)
  • However, a study has been initiated in order to obtain FDA approval, and continued access has been granted by the FDA Based on the approval of Cardiac contractility modulation devices, the therapy is a treatment option for patients that are at least 18 years old who suffer from heart failure symptoms due to left ventricular systolic dysfunction (LVSD) despite adequate medical treatment. (wikipedia.org)
  • Further clinical research are under way to identify which patient group within the scope of the device approval benefits most from Cardiac contractility modulation treatment. (wikipedia.org)
  • Most clinical studies on Cardiac contractility modulation therapy have involved heart failure patients who were classified initially as NYHA Class II, III or IV and had a normal QRS duration (QRS duration ≤ 120 ms). The efficacy of Cardiac contractility modulation on patients in an earlier stage of heart failure has not yet been studied. (wikipedia.org)
  • A subsequent evaluation study (subgroup analysis) has already suggested a particular patient group that responds exceptionally well to Cardiac contractility modulation therapy. (wikipedia.org)
  • Although studies on Cardiac contractility modulation therapy have focused on patients with a normal QRS duration (i.e. ≤ 120 ms), it is possible to use the therapy in patients who meet the treatment indication but who do not have a normal QRS duration. (wikipedia.org)
  • ventricular
  • 1 , 2 Dysregulation of cardiac Ca V 1.2 channels results in life-threatening atrial and ventricular arrhythmias and may contribute to contractile dysfunction in heart failure. (ahajournals.org)
  • Studies have shown celivarone is capable of cardioversion and of maintaining normal sinus cardiac rhythms and that it is effective in hypokalemic, vasotonic, and stretch-induced atrial fibrillation, as well as ischemic and reperfusion ventricular fibrillation. (wikipedia.org)
  • heart's
  • Heart patches, on the other hand, could conceivably be implanted over the dead muscle and remain active for a long time, providing more strength for contractions and a smooth path for the heart's electrical signals to travel through. (scitechdaily.com)
  • By revealing this robust homing mechanism, which causes cardiac stem cells to home to and repair the heart's damaged muscle, the findings could lead to less invasive treatments or even preventative measures aimed at maintaining or increasing the activity of the heart's own cardiac stem cells. (scitechdaily.com)
  • Disruptions in ion flow affect the heart's ability to contract by altering the resting membrane potential, affecting the cell's ability to conduct or transmit an action potential (AP), or by affecting the rate or force of contraction. (wikipedia.org)
  • proteins
  • Diviani D, Maric D, Perez Lopez I et al (2013) A-kinase anchoring proteins: molecular regulators of the cardiac stress response. (springer.com)
  • conduction system
  • The causes of cardiac arrhythmias are numerous, from structural changes in the conduction system (the sinoatrial and atrioventricular nodes, or His-Purkinje system) and cardiac muscle, to mutations in genes coding for ion channels of the heart. (wikipedia.org)
  • In the same way that the walls of a house contain electrical wires and plumbing, cardiac muscle also contains specialised cells for conducting electrical signals rapidly (the cardiac conduction system), and blood vessels to bring nutrients to the muscle cells and take away waste products (the coronary arteries, veins and capillary network). (wikipedia.org)
  • improvement in cardiac
  • This therapy is intended for the treatment of patients with moderate to severe heart failure (NYHA class II-IV) with symptoms despite optimal medical therapy who can benefit from an improvement in cardiac output. (wikipedia.org)
  • pathophysiology
  • The finding that cAMP signalling is compartmentalised and that distinct, spatially segregated pools of cAMP mediate different functional effects in the heart may provide a rationale for what appear to be contrasting effects of this pathway on cardiac physiology and pathophysiology. (springer.com)
  • rhythms
  • Alterations in calcium buffering have been implicated in the tendency to arrhythmias (abnormal cardiac rhythms) in some genetic mutations known to cause hypertrophic cardiomyopathy. (wikipedia.org)
  • cellular
  • If the cardiac stem cells are replaced the heart repairs itself, leading to complete cellular, anatomical and functional heart recovery, with the heart returning to normal and pumping at a regular rate. (scitechdaily.com)
  • Recent evidence indicates that the hemodynamic alterations accompanying heart failure are coincident with a common pattern of electrophysiological and excitation-contraction (E-C) coupling changes at the cellular level. (ahajournals.org)
  • potassium
  • Activation of particular VGCCs allows Ca2+ to rush into the cell, which, depending on the cell type, results in activation of calcium-sensitive potassium channels, muscular contraction, excitation of neurons, up-regulation of gene expression, or release of hormones or neurotransmitters. (wikipedia.org)
  • mitochondria
  • Cardiac muscle cells contain many mitochondria which provide the energy needed for the cell in the form of adenosine triphosphate (ATP), making them highly resistant to fatigue. (wikipedia.org)
  • myosin
  • Omecamtiv mecarbil (INN), previously referred to as CK-1827452, is a cardiac-specific myosin activator. (wikipedia.org)
  • Chemical energy in the form of ATP is converted into mechanical energy which allows myosin to strongly bind to actin and produce a power stroke resulting in sarcomere shortening/contraction. (wikipedia.org)
  • This enhances effective myosin cross-bridge formation and duration, while the velocity of contraction remains the same. (wikipedia.org)
  • cells
  • Fewer than one percent of the injected cells survive and remain in the heart, and even fewer become cardiac muscle cells. (scitechdaily.com)
  • A newly published study shows for the first time that if cardiac stem cells are eliminated, the heart is unable to repair itself after damage. (scitechdaily.com)
  • Also, if the cardiac stem cells are removed and re-injected, they naturally 'home' to and repair the damaged heart, a discovery that could lead to less-invasive treatments and even early prevention of heart failure in the future. (scitechdaily.com)
  • The study, funded by the European Commission Seventh Framework Program (FP7), set out to establish the role of cardiac stem cells (eCSCs) by first removing the cells from the hearts of rodents with heart failure. (scitechdaily.com)
  • In these cases it could be possible to replace the damaged cardiac stem cells or add new ones by growing them in the laboratory and administering them intravenously. (scitechdaily.com)
  • Dr Ellison added: 'Understanding the role and potential of cardiac stems cells could pave the way for a variety of new ways to prevent and treat heart failure. (scitechdaily.com)
  • These new approaches involve maintaining or increasing the activity of cardiac stem cells so that muscle tissue in the heart can be renewed with new heart cells, replacing old cells or those damaged by wear and tear. (scitechdaily.com)
  • The cardiac stem cells naturally home to the heart because the heart is their home - they know to go there. (scitechdaily.com)
  • Next steps include clinical trials, due to start early 2014, aimed at assessing the effectiveness of cardiac stem cells for preventing and treating heart failure in humans. (scitechdaily.com)
  • an important difference is that cardiac cells contract when placed in Na-free salines while skeletal muscle fibers do not. (springer.com)
  • Since in many cardiac cells this sort of replacement does not change membrane potential, one must ask what is the signal for contraction produced by a reduction in external Na. (springer.com)
  • Transverse tubules (T-tubules) are extensions of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells. (wikipedia.org)
  • T-tubules are tubules formed from the same phospholipid bilayer as the surface membrane or sarcolemma of skeletal or cardiac muscle cells. (wikipedia.org)
  • In cardiac muscle cells, T-tubules are between 20 and 450 nanometers in diameter and are usually located in regions called Z-discs where the actin filaments anchor within the cell. (wikipedia.org)
  • In cardiac muscle cells, as the action potential passes down the T-tubules it activates L-type calcium channels in the T-tubular membrane. (wikipedia.org)
  • Viewed through a microscope, cardiac muscle cells are roughly rectangular, measuring 100-150μm by 30-40μm. (wikipedia.org)
  • The regular organisation of myofibrils into sarcomeres gives cardiac muscle cells a striped or striated appearance when looked at through a microscope, similar to skeletal muscle. (wikipedia.org)
  • The cardiac action potential is a brief change in voltage (membrane potential) across the cell membrane of heart cells. (wikipedia.org)
  • The cardiac action potential differs from action potentials found in other types of electrically excitable cells, such as nerves. (wikipedia.org)
  • All cardiac muscle cells are electrically linked to one another, by structures known as gap junctions (see below) which allow the action potential to pass from one cell to the next. (wikipedia.org)
  • action potential
  • Ultimately, muscle contraction revolves around a charged atom (ion), calcium (Ca2+), which is responsible for converting the electrical energy of the action potential into mechanical energy (contraction) of the muscle. (wikipedia.org)
  • The ability for the Na+/Ca2+ exchanger to reverse direction of flow manifests itself during the cardiac action potential. (wikipedia.org)
  • However, during the upstroke of the cardiac action potential there is a large influx of Na+ ions. (wikipedia.org)
  • This is because, the Ca2+ that enters the cell via the DHPR in response to the action potential, stimulates both muscle contraction and calcium release from the SR. The Ca2+ released during the spark, then activates two other ion channels on the membrane. (wikipedia.org)
  • membrane
  • It cannot be electrical since membrane potential does not change and, in spite of some rather exotic ideas that have been put forward, the most viable idea is that if Na o is made low, Ca o can exchange for Na i and thus a flux of inward moving Ca is generated to provide for a contraction. (springer.com)
  • Contrary to findings in reconstituted systems, Rem-induced ablation of cardiac I Ca,L requires GTP-binding, but not membrane-targeting of the nucleotide binding domain. (ahajournals.org)