42 results about "Proarrhythmia" patented technology

An implantable devices for the effective elimination of an arrhythmogenic site from the myocardium is presented. By inserting small biocompatible conductors and / or insulators into the heart tissue at the arrhythmogenic site, it is possible to effectively eliminate a portion of the tissue from the electric field and current paths within the heart. The device would act as an alternative to the standard techniques for the removal of tissue from the effective contribution to the hearts electrical action which require the destruction of tissue via energy transfer (RF, microwave, cryogenic, etc.). This device is a significant improvement in the state of the art in that it does not require tissue necrosis.In one preferred embodiment the device is a non conductive helix that is permanently implanted into the heart wall around the arrhythmogenic site. In variations on the embodiment, the structure is wholly or partially conductive, the structure is used as an implantable substrate for anti arrhythmic, inflammatory, or angiogenic pharmacological agents, and the structure is deliverable by a catheter with a disengaging stylet. In other preferred embodiments that may incorporate the same variations, the device is a straight or curved stake, or a group of such stakes that are inserted simultaneously.

Atrial arrhythmias, a major contributor to cardiovascular morbidity, are believed to be influenced by autonomic nervous system tone. The main purpose of this invention was to highlight new findings that have emerged in the study of effects of autonomic nervous system tone on atrial arrhythmias, and its interaction with class III antiarrhythmic drug effects. This invention evaluates the significance of sympathetic and parasympathetic activation by determining the effects of autonomic nervous system using a vagal and stellar ganglions stimulation, and by using autonomic nervous system neurotransmitters infusion (norepinephrine, acetylcholine). This invention evaluates the autonomic nervous system effects on the atrial effective refractory period duration and dispersion, atrial conduction velocity, atrial wavelength duration, excitable gap duration during a stable circuit (such atrial flutter circuit around an anatomical obstacle), and on the susceptibility of occurrence (initiation, maintenance and termination) of atrial re-entrant arrhythmias in canine. This invention also evaluates whether autonomic nervous system activation effects via a local neurotransimitters infusion into the right atria can alter those of class III antiarrhythmic drug, sotalol, during a sustained right atrial flutter. This invention represents an emergent need to set-up and develop a new class of anti-cholinergic drug therapy for the treatment of atrial arrhythmias and to combine this new anti-cholinergic class to antiarrhythmic drugs. Furthermore, this invention also highlights the importance of a local application of parasympathetic neurotransmitters / blockers and a catheter ablation of the area of right atrium with the highest density of parasympathetic fibers innervation. This may significantly reduce the occurrence of atrial arrhythmias and may preserve the antiarrhythmic effects of any drugs used for the treatment of atrial re-entrant arrhythmias.

The invention relates to a medicinal composition, which consists of the following parts: a calcium ion antagonist (CCB) or pharmaceutically acceptable salt thereof, an angiotensin II acceptor antagonist (ARB) or pharmaceutically acceptable salt or ester thereof, statins or pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier. The invention also relates to a combined kit containing the active substances. The medicinal composition or the kit is used for treating hypertension, dyslipidemia, cerebrovascular disorder, stroke, coronary heart disease, diabetes, diabetic complication, angina, myocardial infarction, cardiac insufficiency, renal dysfunction, atherosclerosis, ventricular hypertrophy, aneurysm, myocardial ischemia, arrhythmia and glaucoma of patients, reducing the incidence rate and / or the death rate of cardiovascular and cerebrovascular disease, improving the adaptability of drug administration of the patients at the same time, and improving the life quality of the patients.

The invention relates to the technical field of biomedical engineering. At present, the research about the construction of a tissue-engineered atrioventricular node is not reported in China and foreign countries. The invention provides a method for constructing the tissue-engineered atrioventricular node by using cardiac pacing cells and conduction cells which are obtained by inducing collagen sponge and bone marrow mesenchymal stem cells. The bone marrow mesenchymal stem cells are induced into the pacing cells through co-culture with sinoatrial node cells, and are induced into the cardiac pacing cells by a method for co-culture with auricular appendage muscle cells; and the two kinds of cells are used as seed cells, the collagen sponge is taken as a bracket, and the tissue-engineered atrioventricular node with a pacing characteristic and an electrocardio-conduction characteristic is constructed in vitro. Through animal experiments, the successfully constructed tissue-engineered atrioventricular node is transplanted to treat atrioventricular conduction block, and a good treatment effect is achieved. The tissue-engineered atrioventricular node which has the electrocardio-conduction characteristic and can be transplanted for treatment is obtained, and hope is brought to treatment of arrhythmia caused by heart atrioventricular conduction block.

A leveo-potassium magnesium aspartate infusion injection consists of levo-potassium aspartate, levo-magnesium asparatate, osmotic pressure regulator and pH regulator. It is a kind of electrolyte extender for infusion, and has pH value of 5-11.5, high concentration, large dosage, high stability and no pollution. it has wide application range, and is suitable for intravenously guttae to treat arrhythmia caused by various causes, chronic alcoholism fremitus, myocardiopathy as diabetes complication, etc. and applicaltion in heart operation. It is also suitable for acute and chronic hepatitis, intrahepatic cholestasis, and disease of respiratory system, nerve system and metabolic system.

The present invention discloses one kind of benzimidazole compound and its prepare and application in producing medicine. The compound has the general expression as shown. The compound is potassium ion channel retardant, has arrhythmia treating activity and no side effect, and may be used in preparing medicine for arrhythmia. The preparation process has facile material and mild reaction condition.

Disclosed are methods of terminating acute episodes of cardiac arrhythmia, such as atrial fibrillation or ventricular fibrillation, in a mammal, such as a human, by administering to that mammal an amount of domperidone, or a pharmaceutically acceptable salt, derivative or metabolite thereof, effective to terminate an acute episode of cardiac arrhythmia and / or restore normal sinus rhythm or heart rate. Also disclosed are methods of maintaining normal sinus rhythm or heart rate in a mammal, such as a human, and preventing a recurrence of an episode of cardiac arrhythmia in a mammal, by administering an amount of domperidone, or a pharmaceutically acceptable salt, derivative or metabolite thereof, effective to maintain normal sinus rhythm or heart rate in a mammal that has experienced at least one prior episode of cardiac arrhythmia. Pharmaceutical compositions for use in these methods are also disclosed.

The invention relates to stephanine and its pharmaceutically acceptable salt and an application of a solvate for preparing an antiarrhythmic medicine, which belongs to the technical field of medicine. A structural formula of stephanine is shown as a formula (I); the researches on chloroform-induced mice arrhythmia show that stephanine can resist chloroform-induced ventricular fibrillation, preliminary determination is confirmed that the stephanine has antiarrhythmic effect; then barium chloride-induced rat ventricular rhythm test, aconitine intravenous injection-induced rat cardiac rhythm test and rat myocardial ischemia and ischemia reperfusion arrhythmia test are carried out, so that stephanine has good antiarrhythmic effect, and provides a good base for preparing various antiarrhythmic medicines next time.

Disclosed herein is the method for synthesis and separation of enantiospecific isomers of floxacins. These isomers can be used to study the antibacterial action, as well as cardiac effects, such as arrhythmogenic activity, QT internal prolongation and dispersion, and Ikr inhibition in humans. A method for the identification of chiral isolates of the floxacins that are devoid or possess less QT prolonging action and thus cause less arthropathy especially of the Torsades de pointes variety. Also disclosed are methods for assaying these isomeric compounds present in the biological fluids.

The invention relates to the medicine field, particularly relating to a drug for treating arrhythmia, in particular to an application of Zacopride in preparing a drug for treating the arrhythmia. The invention aims at solving the problems that the present antiarrhythmic drugs have the effect of causing arrhythmia, and IK1 selective agonist has not been discovered at home and abroad so far. The Zacopride is an IK1 selective agonist which is discovered at present for the first time and is used on an antiarrhythmic drug. Used as a drug for treating ischemia-reperfusion arrhythmia, the Zacopride has the similar effect to that of lidocaine, takes effect stably and does not obviously affect the rhythm with wide safety range. In the experiments of arrhythmia induced by ischemia-reperfusion, lidocaine can make the rhythm slower, while the Zacopride has no obvious effect; and when the dosage of the lidocaine is increased by one-third, the antiarrhythmic effect is obviously weakened, while such phenomenon occurs when the Zacopride reaches one hundred times of effective concentration.

A device, system, and method for delivering energy to tissue. In particular, the present invention relates to a system and method for enhancing lesion formation without arrhythmogenic effects within relatively thick target tissues, such as the ventricles of the heart. In one embodiment, charge-neutral pulses and non-charge-neutral pulses may be delivered to induce the formation of electrolytic compounds that enhance cell death at the treatment site. Additionally or alternatively, tissue at the treatment site may be heated to sub-lethal temperature before ablating the tissue.

The present invention relates to short-acting calcium channel blocking compounds and their use to treat ischemic heart conditions, cardiac arrhythmias, hypertensive crisis in an emergency room setting, hypertension in general, hypertension been.) fore, during, or after surgery, no-reflow phenomenon following reperfusion, and diseases associated with decreased skeletal muscle blood flow. The invention also relates to pharmaceutical compositions formulated for use in such methods and to kits for such methods.

Skeletal myoblasts are an attractive cell type for transplantation since they are autologous and resistant to ischemia. However, clinical trials of myoblasts transplantation in heart failure have been plagued by ventricular tachy-arrhythmias and sudden cardiac death. The pathogenesis of these arrhythmias is poorly understood, but may be related to the fact that skeletal muscle cells, unlike heart cells, are electrically isolated by the absence of gap junctions. An in vitro model of myoblasts transplantation into cardiomyocyte monolayers can be used to investigate the mechanisms of transplant-associated arrhythmias. Co-cultures of human skeletal myoblasts and rat cardiomyocytes result in reentrant arrhythmias (spiral waves) that reproduce the features of ventricular tachycardia seen in patients receiving myoblasts transplants. These arrhythmias can be terminated by nitrendipine, an L-type calcium channel Mocker, but not by the Na channel blocker lidocaine. Genetic modification of myoblasts to stably express the gap junction protein connexin 43 decreases arrhythmogenicity in co-cultures. It similarly can be used to increase the safety of myoblasts transplantation in patients.

The invention relates to purposes of polygonum cuspidatum extract, namely polydatin. Myocardial hypertrophy is the most important reason for triggering congestive heart failure. Ventricular hypertrophy usually involves ventricular structure change, namely ventricular remodeling. The ventricular remodeling is a complication of multiple cardiovascular diseases and a vital and decisive element in the development process of the congestive heart failure. The arrhythmia occurrence rate after the myocardial remodeling is increased by 28%, and cardiac sudden deaths caused in the end are increased by over five times. It is indicated that through in vitro study tests, the polydatin remarkably restrains heart ion channels caused by ischemia indury of mice from remodeling and has a great protective effect for arrhythmia, and therefore the polydatin can be used for preparing products resisting against arrhythmia caused by myocardial hypertrophy and / or ventricular hypertrophy. According to the method, the polydatin plays the anti-arrhythmic role by increasing the electric current density of transient outward potassium current (Ito), shortening the action potential duration (APD) of cardiac muscle cells and restraining the QT inter-phase from being prolonged.

Provided are a model animal physiologically similar to humans, enabling a highly reproducible evaluation of the onset of drug-induced long QT syndrome, a method of generating the same, and an evaluating method using the same. A proarrhythmia model animal of a monkey, prepared by ablating the atrioventricular node; the foregoing monkey is preferably a cynomolgus monkey. A method of generating a proarrhythmia model animal, comprising a step for inserting an electrode catheter to the heart of a monkey, and ablating atrioventricular node with the catheter, and a method of evaluating the QT interval prolongation by a drug, comprising using the foregoing model animal.

The embodiment of the invention provides an electrocardiosignal processing method and device, a terminal and a storage medium. The method comprises the following steps of continuously acquiring an electrocardiosignal from an electrocardiogram monitor; intercepting an electrocardiosignal segment with a preset time length from the electrocardiosignal; determining at least one candidate QRS wave in the electrocardiosignal segment; removing a noise QRS wave in the at least one candidate QRS wave to obtain a target QRS wave; and detecting whether an arrhythmia event occurs to the electrocardiosignal segment based on the target QRS wave. According to the technical scheme provided by the embodiment of the invention, the long-term electrocardiosignal is intercepted into the short electrocardiosignal, the QRS wave is determined in the short electrocardiosignal segment, and whether the arrhythmia event occurs or not is detected based on the QRS wave, so that the occurrence of the situation that the arrhythmia event cannot be timely detected after the long-term electrocardiosignal is analyzed is avoided, and the detection efficiency of the arrhythmia event is improved.

The invention provides application of sodium houttuyfonate to preparation of a medicament for treating heart failure and / or arrhythmia. The invention also provides application of the sodium houttuyfonate to preparation of a medicament for enhancing contractile force of ventricular myocytes. The sodium houttuyfonate increases L-type calcium current (Ica.L), and can improve myocardial systolic dysfunction caused by the reduction of sarcoplasmic reticulum Ca release when the heart failure is occurred. The sodium houttuyfonate blocks peak sodium current (Ina.p) and has the characteristics of class-I antiarrhythmic medicaments, and can also block late sodium current (INa.L) increased by the induction of congestin II (ATX-II) and has the potential of inhibiting the arrhythmia caused by the increment of the INa.L.

Compositions for intravenous infusion of istaroxime, or a metabolite of istaroxime, in human patients suffering from heart failure are disclosed. Likewise, methods for extended infusion of istaroxime or its metabolites in individuals with heart failure are disclosed. In particular, some methods disclosed herein include the infusion of istaroxime, or a metabolite thereof, for a period of time that is greater than six hours in order to improve cardiac relaxation without triggering arrhythmogenic events in an individual suffering from heart failure. Other methods include administration of istaroxime until certain plasma concentration thresholds of istaroxime metabolites are achieved. Also disclosed are istaroxime metabolites with selective SERCA2a activation.

Disclosed in certain embodiments is a method of treating an arrhythmia comprising administering to a patient in need thereof an effective amount of an opioid antagonist to treat the arrhythmia.

The invention discloses a new application of tanshinone IIA. Tanshinone IIA is one of main effective components in tanshinone, has a quinoid structure, is easy to be oxidized and reduced, can participate in various biochemical reactions in human body and has various biological activities. Tanshinone IIA has various pharmacological effects, can resist cardiac muscle acute hypoxic injury, resist arrhythmia, improve blood vessel smooth muscle functions, and has protection effect on tissue damage caused by ischemia-reperfusion. According to the invention, tanshinone IIA can reduce the arsenic content in body blood. Arsenic is a toxic substance with severe harm to human body. Research shows that when compared with a blank control group, rats administrated with tanshinone IIA have obviously reduced arsenic concentration in blood.

The invention discloses novel application of nifekalant to preparation of medicine for treating supraentricular arrhythmias. An intravenous medicated medicine is prepared from the medicine containing the nifekalant with clinical effective dose as the unique activating agent. At least one new application of the nifekalant is developed through preparing the nifekalant into medicines for treating atrial fibrillation, atrial flutter and other supraentricular arrhythmias, and the medicinal application range of the nifekalant is increased and more patients with atrial fibrillation, atrial flutter and other supraentricular arrhythmias can received better treatment. The medicine can reduce the recurernce rate of the supraentricular arrhythmias, and improve all vital signs, and surviving rate of the patients.

The invention relates to the technical field of biomedical engineering. At present, the research about the construction of a tissue-engineered atrioventricular node is not reported in China and foreign countries. The invention provides a method for constructing the tissue-engineered atrioventricular node by using cardiac pacing cells and conduction cells which are obtained by inducing collagen sponge and bone marrow mesenchymal stem cells. The bone marrow mesenchymal stem cells are induced into the pacing cells through co-culture with sinoatrial node cells, and are induced into the cardiac pacing cells by a method for co-culture with auricular appendage muscle cells; and the two kinds of cells are used as seed cells, the collagen sponge is taken as a bracket, and the tissue-engineered atrioventricular node with a pacing characteristic and an electrocardio-conduction characteristic is constructed in vitro. Through animal experiments, the successfully constructed tissue-engineered atrioventricular node is transplanted to treat atrioventricular conduction block, and a good treatment effect is achieved. The tissue-engineered atrioventricular node which has the electrocardio-conduction characteristic and can be transplanted for treatment is obtained, and hope is brought to treatment of arrhythmia caused by heart atrioventricular conduction block.

A novel application of niflumic acid (NFA) in treating arrhythmia is disclosed. It can block the chlorine ion channel to treat the arrhythmia caused by low osmotic pressure and aconitine. It can be also used for auxiliary therapy of hypertension.

The subject invention provides useful and novel calcium channel blockers based upon mibefradil. The subject invention also provides methods for synthesizing the compounds of the invention. The invention also provides methods for the control or prevention of hypertension, angina pectoris, ischemia, arrhythmias, and cardiac insufficiency in a patient by administering a compound, or composition, of the invention to an individual in need of such treatment.