9 results about "Ventricular hypertrophy" patented technology

A method of cardiac treatment to provides a synergetic therapeutic effect of lowering the hyperactive sympathetic response observed in microvascular disease (MVD) and heart failure (HF) pathologies and promoting cardiac remodeling of left ventricular hypertrophy in a patient. The method may include ablating renal sympathetic nerves of the patient to reduce sympathetic afferent and efferent activity to the kidney, thereby reducing blood pressure, delivering cardiac pacing to induce remodeling of hypertrophy of the left ventricle of the patient's heart, and stimulating a vagus nerve of the patient to induce an anti-inflammatory reflex in the patient's heart. The method may include ablating renal sympathetic nerves of the patient to reduce sympathetic afferent and efferent activity to the kidney, thereby reducing blood pressure, and stimulating carotid baroreceptors of the patient to downregulates sympathetic tone and upregulates parasympathetic tone.

The application belongs to the technical field of molecular biology, and particularly relates to metabolic markers for distinguishing hypertrophic cardiomyopathy and left ventricular hypertrophy and application. The application analyzes the metabolome of hypertrophic cardiomyopathy (HCM) patients, left ventricular hypertrophy (LVH) patients caused by non-hypertrophic cardiomyopathy and healthy people, finds that carnitine C16:2, carnitine C14:0, carnitine C16:0, carnitine C18:0 and carnitine C18:1 are differentially expressed in HCM patients and LVH patients, pyridoxine phosphate, ito acid, adenosine monophosphate, adenosine diphosphate and adenosine triphosphate are differentially expressed in HCM patients and healthy people, lysine base, methyl glutamic acid, acetyl proline, malate semialdehyde and citramalate are differentially expressed in LVH patients and healthy people, and ROC curve analysis shows excellent prediction effect, strong specificity and high sensitivity.

Disclosed are systems and methods that can differentiate between disease states using ECG data analyzed via dynamic control analysis. In some embodiments, the disease states are Hypertrophic Cardiomyopathy (HCM) and Left Ventricular Hypertrophy. In some embodiments, the exemplary system and method is configured to transform ECG data in the time domain into complex numbers in the frequency domain (s-domain). A pattern recognition or AI classifier can then find patterns of the complex numbers in the s-domain to differentiate between the disease states (e.g., HCM and LVH).

Methods and materials for treating chronic cardiac disorders are provided herein. For example, methods and materials for using a dual guanylate cyclase A and B activator (e.g., a polypeptide having the sequence set forth in SEQ ID NO:1) to treat hypertrophic cardiomyopathy and other cardiac conditions, such as conditions associated with ventricular hypertrophy, atrial hypertrophy, ventricular remodeling, atrial remodeling, systolic and / or diastolic dysfunction, heart failure (e.g., heart failure with reduced ejection fraction, heart failure with mildly reduced ejection fraction, and heart failure with preserved ejection fraction), and other forms of chronic heart disease (e.g., Fabry disease, Noonan syndrome, Pompe disease, PRKAG2-related cardiomyopathy, Danon disease, Friedrich ataxia cardiomyopathy, amyloidosis, or desminopathy) are provided herein.

The present disclosure lies in the general field of clinical electrocardiography (ECG), more specifically in ECG methods comprising precordial ECG amplitude measurements. The present invention relates to methods of determining a subject's corrected precordial ECG amplitude from an ECG measurement, which corrections are based on intraindividual changes such as the rotation position of the heart on the horizontal plane, and / or changes in body mass index. The methods are thus useful for adjustment of intraindividual changes over time in precordial ECG amplitudes, such as between two ECG measurements. The present invention further relates to a device, an apparatus and a computer program product, and to uses of said device, apparatus and computer program product in a method of determining a subject's corrected precordial ECG amplitude from an ECG measurement, and for improving the accuracy of electrocardiographic methods depending on precordial ECG amplitude measurements. For example, the methods and the device, apparatus or product can be advantageously used in a method of diagnosing left ventricular hypertrophy and / or hypertension in a subject.

The invention provides application of a Phb2 inhibitor YL-939 in preparation of a medicine for treating pulmonary arterial hypertension, and relates to the technical field of medicine development. In the pulmonary arterial hypertension disease process, the histone lactylation level is remarkably increased, and the Phb2 can be used as a histone lactylation modifying enzyme for up-regulating expression in pulmonary arterial hypertension and playing an important role, and can lead to abnormal proliferation of vascular smooth muscle cells and pathological change of vascular walls by promoting histone lactylation modification. Through targeted inhibition of Phb2, pulmonary artery blood vessel middle layer thickening can be significantly relieved, the small artery myelization degree can be reduced, extravascular collagen deposition can be inhibited, and thus pulmonary circulation dynamics can be improved. As a Phb2 inhibitor, YL-939 can effectively relieve ventricular hypertrophy caused by pulmonary arterial hypertension, has no obvious toxic or side effect, and shows unique advantages and good application prospects in the aspect of treating pulmonary arterial hypertension.

Disclosed herein are techniques for evaluating cardiac health of a pediatric patient or adult congenital patient, including techniques for generating one or more models (e.g., machine learning models) trained to predict a cardiac abnormality in a pediatric patient or adult congenital patient. Some methods may include receiving electrocardiogram (ECG) data of a pediatric patient or adult congenital patient, determining whether the patient corresponds to one or more of multiple cardiac phenotypes, each corresponding to a presence of a cardiac abnormality based on analysis by one or more trained models, and outputting the cardiac phenotype(s) based on the ECG data. In some embodiments, the cardiac abnormality may include one or more of mortality, ventricular dysfunction, ventricular dilation, ventricular hypertrophy, one or more rhythm abnormality, one or more ECG abnormality, and critical congenital heart disease.

There was a need for safe and effective treatments for pulmonary hypertension, especially pulmonary arterial hypertension (PAH). The inventors discovered dysregulation of the kynurenine pathway (KP) in the lungs of PAH patients, marked by an imbalance of KP metabolites and upregulation of key enzymes, particularly kynurenine 3-monooxygenase (KMO). This disclosure pertains to a kynurenine-3-monooxygenase inhibitor for use in the treatment or prevention of pulmonary hypertension, in particular pulmonary arterial hypertension. The kynurenine-3- monooxygenase inhibitor is effective in reducing vascular and cardiac remodeling, decreasing right ventricular systolic pressure, reducing pulmonary ventricular resistance, decreasing medial hypertrophy of large arteries, lowering the proportion of muscularized and occluded small arteries and decreasing right ventricular hypertrophy.

Disclosed are methods and agents for treating heart failure. More particularly, the present disclosure relates to the use of CD14 antagonist antigen-binding molecules for treating heart failure, including alleviating, reducing or reversing adverse cardiac structural remodeling, improving cardiac contractile function, improving ejection fraction (e.g., left ventricular ejection fraction), left ventricular end-systolic volume, left ventricular end- diastolic volume, left ventricular akinesia, left ventricular dilatation, and / or left ventricular hypertrophy, reducing dyspnea, improving congestion score and / or patient perception of their health status and / or reducing neutrophil / lymphocyte ratio.