Arrhythmias in Hypertrophic Cardiomyopathy and Their Management
Srilakshmi M. Adhyapak, V. Rao Parachuri in Hypertrophic Cardiomyopathy, 2020
Hypertrophic cardiomyopathy is the commonest form of hereditary heart disease, with a prevalence of 1 in 500 people [3]. Atrial fibrillation is the most prevalent sustained arrhythmia in both HCM and the general population, though it occurs at a four to six times higher rate in the former than the latter [4]. In a meta-analysis of 7,381 patients, the overall AF prevalence in HCM patients was 22.5%, and incidence was 3.1% per 100 patients per year [5]. Approximately two-thirds of AF is paroxysmal in HCM while the remainder are persistent or permanent [6]. Furthermore, a greater number of people have silent AF, at 24% in one study, which can then progress into symptomatic overt AF [7]. Other forms of atrial tachyarrhythmias, such as atrial flutter, atrial tachycardia, atrioventricular re-entrant tachycardia, and atrioventricular nodal re-entrant tachycardia, can all occur in HCM and share some of the clinical implications with AF [2].
Cardiomyopathies in Pregnancy
Afshan B. Hameed, Diana S. Wolfe in Cardio-Obstetrics, 2020
Family-based studies suggest a familial relationship in 20%–35% of patients diagnosed with DCM [26]. Most are transmitted as autosomal dominants, although all inheritance patterns are described. Genetic studies have identified mutations in more than 30 genes [26]. Estimated incidence is approximately 1:2500 [1]. Most patients will have an initial diagnosis of idiopathic cardiomyopathy. Diagnosis of familial DCM requires presence of LV dilatation and impaired systolic function in one or both ventricles in two or more closely related family members [27]. Mutation-specific genetic testing is recommended for family members when a DCM causative mutation is found in the index case even in the absence of symptoms [5]. Clinical manifestations of familial DCM are similar to other idiopathic DCM. General risks to be considered include progressive LV dysfunction which can be severe enough to require transplantation, arrhythmias including sudden cardiac death and, if pregnancy is pursued, transmission to offspring. Outcome data on pregnancy in women with familial DCM is extrapolated from a small cohort series of women with idiopathic DCM [20,22–25,28].
Diabetic Cardiomyopathy: Present Status and Future Directions
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla in Heart Dysfunction in Diabetes, 2019
Since diabetes is a complex disease, no simple therapy may prove useful in preventing or reversing the diabetic cardiomyopathy. Obviously, insulin remains as the intervention of choice and other drugs should supplement this hormone. Animal studies have provided some important clues that the sympathetic nervous system is activated at early stages of diabetes. Accordingly, ganglionic blocking drugs and β-adrenergic blocking agents may prove useful at initial stages. Since high levels of circulating catecholamine in diabetic patients may become oxidated to toxic products which may induce cardiomyopathy, it may prove beneficial to use antioxidant agents in chronic cases of diabetes. As diabetic cardiomyopathy has been shown to involve the occurrence of intracellular Ca2+-overload, the use of Ca2+-antagonist agents can also be seen to produce beneficial effects. In view of the importance of cholesterol in inducing cardiovascular dysfunction, the use of cholesterol-lowering agents cannot be overlooked. Furthermore, different metabolic interventions which are known to promote the energy status of myocardium could delay or prevent the occurrence of cardiomyopathy in diabetes, which is known to alter cellular metabolism in a complex manner. Thus it appears that a combination drug therapy, depending upon the stage of disease and other clinical abnormalities which may be present in the diabetic patient, may prove most useful for diabetic cardiomyopathy.
Left ventricular long-axis ultrasound strain (GLS) is an ideal indicator for patients with anti-hypertension treatment
Published in Clinical and Experimental Hypertension, 2022
Tingting Wu, Lulu Zheng, Saidan Zhang, Lan Duan, Jing Ma, Lihuang Zha, Lingfang Li
The Research Ethics Committee of the Xiangya Hospital of Central South University had approved this study. All participating members had carefully read and signed informed consent. All enrolled members were divided into three groups, including 1) hypertensive treatment experimental group: 56 patients with newly diagnosed essential hypertension were followed up. 3) Healthy control group: 37 normal volunteers from the physical examination center were collected. The inclusion criteria are as follows: 1) Newly diagnosed essential hypertension. The diagnostic criteria included not taking antihypertensive drugs, measuring blood pressure three times on a different day, systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg (14); 2) 2) Patients with the previous diagnosis of hypertension and poor blood pressure control. After taking antihypertensive drugs, blood pressure was measured three times on a different day. The systolic blood pressure ≥140 mmHg and/or diastolic blood pressure≥90 mmHg. Moreover, exclusion criteria were as follows: 1) Patients have diagnosed as coronary heart disease; 2) Patients with various types of valvular heart disease; 3) Patients with various types of cardiomyopathy; 4) Patients with atrial fibrillation and atrial flutter; 5) Patients were previously diagnosed with primary and secondary pulmonary hypertension; 6) Patients with secondary hypertension; 7) LVEF <50% of patients with hypertension; 8) Patients with diabetes; 9) Patients with atrioventricular block of
The lethal effects and determinants of microcystin-LR on heart: a mini review
Published in Toxin Reviews, 2021
Muwaffak Alosman, Linghui Cao, Isaac Yaw Massey, Fei Yang
Cardiomyopathy occurs as a result of damage heart muscle, which leads to disturbance in the heart of pumping action, and consequent heart failure. As mentioned previously, high dose of MC-LR induce myocardial damage, and cardiotoxicity of MC-LR can cause intracellular oxidative stress imbalance, which may lead to neutrophil inflammatory infiltration, increase protease secretion, and produce a large number of oxidative intermediate products. This may induce cardiopathy (Ding and Ong 2003). As explained earlier, the operating mechanism of MC-LR toxicity is increasing the production of reactive oxygen species (ROS) and impeding the normal functioning of both PP-1 and PP-2A. La-Salete et al. (2008) indicated that the toxicity further interacts with aldehyde dehydrogenase, synthases mechanism of mitochondrial ATP, and mitochondrial oxidative phosphorylation leading to cardiomyopathy and heart failure.
AL type cardiac amyloidosis: a devastating fatal disease
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Adeel Nasrullah, Anam Javed, Thejus T Jayakrishnan, Aaron Brumbaugh, Ariel Sandhu, Brent Hardman
Clinical presentation of AL type cardiac amyloidosis is varied based on the involved site. Fatigue and weakness are the most common presenting symptoms. Restrictive cardiomyopathy presents with signs and symptoms of diastolic heart failure and decreased exercise tolerance. With progression of the disease, atrial dilation occurs, which predisposes patients to atrial fibrillation and further sequelae of clot formation and systemic embolization. Cardiac conduction may be disrupted by amyloid deposition, often causing a variety of heart blocks. Soft tissue involvement has been seen as periorbital ecchymosis and macroglossia in 12.5% and 27.2%, respectively [7]. Renal AL amyloid can cause myeloma kidney and nephrotic syndrome. With underlying kidney disease, the patient may develop progressive renal failure requiring renal replacement therapy, as seen in the present case. Similar deposits in the liver and peripheral nerves can present as hepatomegaly, transaminitis, and peripheral neuropathy, respectively.
Related Knowledge Centers
- Arrhythmia
- Cardiac Arrest
- Dilated Cardiomyopathy
- Edema
- Fatigue
- Shortness of Breath
- Syncope
- Cardiac Muscle
- Heart Failure
- Hypertrophic Cardiomyopathy
- Shortness of Breath