scholarly journals THE EFFECTS OF SLEEP APNEA ON MARKERS OF CARDIAC MYOCYTE INJURY IN HYPERTROPHIC CARDIOMYOPATHY

2021 ◽  
Vol 77 (18) ◽  
pp. 865
Author(s):  
Sai Swetha Alladi ◽  
Shahid Karim ◽  
Shreyas Venkataraman ◽  
Naima Covassin ◽  
Jan Bukartyk ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Hypertrophic Cardiomyopathy ◽  
Cardiac Myocyte ◽  
Myocyte Injury

Abstract 236: Obstructive Sleep Apnea in Hypertrophic Cardiomyopathy: Comparing Exercise Tolerance, Cardiac Remodeling, Clinical and Genetic Data

2014 ◽  
Vol 7 (suppl_1) ◽  
Author(s):  
Suwen Kumar ◽  
Benjamin Ebner ◽  
Jeniffer Bragg-Gresham ◽  
Peter Farrehi ◽  
Sharlene Day
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Hypertrophic Cardiomyopathy ◽  
High Risk ◽  
Cardiac Remodeling ◽  
Exercise Tolerance ◽  
Functional Class ◽  
Nyha Functional Class ◽  
Obstructive Sleep ◽  
Lv Mass

Background: Prevalence of obstructive sleep apnea (OSA) in hypertrophic cardiomyopathy (HCM) is estimated between 32% and 71%. Individuals with HCM and OSA have increased blood pressure, BMI, , ascending aorta size, left atrial size, left ventricular end diastolic diameter, E/e’ ratio, atrial fibrillation rates and NYHA functional class. It has been suggested that treatment of OSA can decrease the need for septal reduction. However, studies have found no effect of OSA on septal thickness or outflow gradient. It is not known how OSA affects exercise performance or cardiac remodeling assessed by MR. Genetic propensity toward OSA in HCM has not been reported. We propose that OSA predicts decrease exercise tolerance and that cardiac remodeling could be identified using MR. We sought to report on HCM genotype in OSA as well as compare our clinical and echo data with other investigators. Methods: Subjects were identified through our institution’s HCM database. They were surveyed using the STOP-BANG (SB) questionnaire, a validated questionnaire to identify individuals at high risk for OSA. We stratified patients into high risk (HR) and low risk (LR) groups, based on a cut point of greater than or equal to 3 on SB. Demographics and clinical characteristics were extracted from our database. Prevalence and means were compared between the two groups, using Chi-square and t-tests. Differences between the groups were adjusted for age, sex, and BMI using linear mixed models for continuous measures and logistic regression for dichotomous measures. Results: There were 206 respondents, of those 160 (78%) scored high risk for OSA, 60 of which had a history of polysomnogram (PSG) confirming OSA. Having a HR vs. LR SB was associated with a significantly greater likelihood of stroke, CHF hospitalization, NYHA functional class >2, reduced peak VO2, reduced anaerobic threshold and increased LA diameter. Adjusted comparisons for age, gender, and BMI showed that had significantly higher PAWP and LV mass index. Of those with a prior diagnosis of OSA we compared therapy compliant and non-compliant individuals and found they differed on LV mass index (HR=98.7 g/m2 vs. LR=62.0 g/m2, p=0.01). Conclusions: OSA occurs frequently in HCM and is associated with decreased exercise tolerance, worse hemodynamics, poor outcome as well as increased LV mass, which may be attenuated by therapy. OSA is an important and modifiable risk factor in HCM. Prospective evaluation utilizing PSG based diagnosis and positive pressure therapy is warranted.

scholarly journals Characterization and validation of a preventative therapy for hypertrophic cardiomyopathy in a murine model of the disease

2020 ◽  
Vol 117 (37) ◽  
pp. 23113-23124
Author(s):  
Helena M. Viola ◽  
Ashay A. Shah ◽  
Victoria P. A. Johnstone ◽  
Henrietta Cserne Szappanos ◽  
Mark P. Hodson ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Hypertrophic Cardiomyopathy ◽  
Mitochondrial Membrane Potential ◽  
Metabolic Activity ◽  
Murine Model ◽  
Mitochondrial Membrane ◽  
Cardiac Myocyte ◽  
Human Condition ◽  
Preventative Therapy

Currently there is an unmet need for treatments that can prevent hypertrophic cardiomyopathy (HCM). Using a murine model we previously identified that HCM causing cardiac troponin I mutation Gly203Ser (cTnI-G203S) is associated with increased mitochondrial metabolic activity, consistent with the human condition. These alterations precede development of the cardiomyopathy. Here we examine the efficacy of in vivo treatment of cTnI-G203S mice with a peptide derived against the α-interaction domain of the cardiac L-type calcium channel (AID-TAT) on restoring mitochondrial metabolic activity, and preventing HCM. cTnI-G203S or age-matched wt mice were treated with active or inactive AID-TAT. Following treatment, targeted metabolomics was utilized to evaluate myocardial substrate metabolism. Cardiac myocyte mitochondrial metabolic activity was assessed as alterations in mitochondrial membrane potential and flavoprotein oxidation. Cardiac morphology and function were examined using echocardiography. Cardiac uptake was assessed using an in vivo multispectral imaging system. We identified alterations in six biochemical intermediates in cTnI-G203S hearts consistent with increased anaplerosis. We also reveal that AID-TAT treatment of precardiomyopathic cTnI-G203S mice, but not mice with established cardiomyopathy, restored cardiac myocyte mitochondrial membrane potential and flavoprotein oxidation, and prevented myocardial hypertrophy. Importantly, AID-TAT was rapidly targeted to the heart, and not retained by the liver or kidneys. Overall, we identify biomarkers of HCM resulting from the cTnI mutation Gly203Ser, and present a safe, preventative therapy for associated cardiomyopathy. Utilizing AID-TAT to modulate cardiac metabolic activity may be beneficial in preventing HCM in “at risk” patients with identified Gly203Ser gene mutations.

scholarly journals MicroRNA-150 aggravates H2O2-induced cardiac myocyte injury by down-regulating c-myb gene

2013 ◽  
Vol 45 (9) ◽  
pp. 734-741 ◽  
Author(s):  
X. Li ◽  
M. Kong ◽  
D. Jiang ◽  
J. Qian ◽  
Q. Duan ◽  
...  
Keyword(s):  
Cardiac Myocyte ◽  
Myb Gene ◽  
Myocyte Injury

Peroxynitrite-induced cardiac myocyte injury

1996 ◽  
Vol 20 (3) ◽  
pp. 343-350 ◽  
Author(s):  
Hideyuki Ishida ◽  
Kohji Ichimori ◽  
Yuki Hirota ◽  
Masami Fukahori ◽  
Hiroe Nakazawa
Keyword(s):  
Cardiac Myocyte ◽  
Myocyte Injury

Association between obstructive sleep apnea and metabolic abnormalities in patients with hypertrophic cardiomyopathy

2021 ◽  
Author(s):  
Juan Wang ◽  
Haobo Xu ◽  
Jiansong Yuan ◽  
Chao Guo ◽  
Fenghuan Hu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Hypertrophic Cardiomyopathy ◽  
High Density Lipoprotein ◽  
Fasting Glucose ◽  
Density Lipoprotein ◽  
Metabolic Abnormalities ◽  
Obstructive Sleep

Abstract Objectives Metabolic abnormalities have been associated with long-term cardiac mortality in patients with hypertrophic cardiomyopathy (HCM). Obstructive sleep apnea (OSA) is a risk factor for metabolic abnormalities in general populations, but association between OSA and metabolic abnormalities in HCM is still undefined. This study aimed to investigate the relationship between OSA and metabolic dysfunction in a large series of patients with HCM. Methods A total of 587 patients with HCM who underwent sleep evaluations at Fuwai Hospital were included. Data from clinical characteristics, polysomnography studies and metabolic measurements were collected. Results OSA was present in 344 patients (58.6%). Patients with OSA were older, more often male and had more clinical comorbidities. Body mass index, blood pressure, fasting glucose and triglycerides all increased (all P<0.001) and high-density lipoprotein cholesterol decreased (P=0.046) with the severity of OSA. In multivariate analysis, moderate to severe OSA and Log (AHI[apnea-hypopnea index]+1) were independently associated with obesity (OR, 2.42; 95%CI [1.48–3.95] and OR, 1.60; 95%CI [1.31–1.95]), elevated blood pressure (OR, 1.99; 95%CI [1.42–3.26] and OR, 1.31; 95%CI [1.08–1.60]) and elevated triglycerides (OR, 1.71; 95%CI [1.05–2.78] and OR, 1.24; 95%CI [1.02–1.51] but not elevated fasting glucose (OR, 0.88; 95%CI [0.50–1.52] and OR, 1.02; 95%CI [0.82–1.28]) and reduced high-density lipoprotein cholesterol (OR, 1.30; 95%CI [0.83–2.04] and OR, 1.06; 95%CI [0.89–1.27]). Conclusions Severity of OSA is independently associated with some profiles of metabolic abnormalities. Clinical trials are required to determine whether OSA treatment improves metabolic abnormalities and long-term outcomes in patients with HCM.

Patients With Hypertrophic Cardiomyopathy And Obstructive Sleep Apnea Are Not Sleepy

2012 ◽  
Author(s):  
Flávia B. Nerbass ◽  
Rodrigo P. Pedrosa ◽  
Pedro R. Genta ◽  
Murillo O. Antunes ◽  
Edmundo Arteaga-Fernandez ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Hypertrophic Cardiomyopathy ◽  
Obstructive Sleep

Obstructive sleep apnea and hypertrophic cardiomyopathy: A common and potential harmful combination

2013 ◽  
Vol 17 (3) ◽  
pp. 201-206 ◽  
Author(s):  
Flávia B. Nerbass ◽  
Rodrigo P. Pedrosa ◽  
Naury J. Danzi-Soares ◽  
Luciano F. Drager ◽  
Edmundo Arteaga-Fernández ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Hypertrophic Cardiomyopathy ◽  
Obstructive Sleep

Sudden Cardiac Death: A Modern Pathology Approach to Hypertrophic Cardiomyopathy

2015 ◽  
Vol 139 (3) ◽  
pp. 413-416 ◽  
Author(s):  
Linda Kocovski ◽  
John Fernandes
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Cardiac Myocyte ◽  
Clinical Symptoms ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Exertional Dyspnea ◽  
Left Ventricular Outflow ◽  
Cardiac Myocyte Hypertrophy

Hypertrophic cardiomyopathy is one of the most common causes of sudden cardiac death among young adults and adolescents. Unfortunately, the first manifestation of the condition may be sudden death during exertion, such as sporting activities. Other clinical symptoms include exertional dyspnea, angina, and syncope. Postmortem examination often reveals asymmetrical septal thickening and mural plaque formation in the left ventricular outflow tract. Histologic analysis shows cardiac myocyte hypertrophy, myofiber disarray, and interstitial and replacement fibrosis. Molecular analysis for known genetic abnormalities is essential to genetic counseling of living relatives of decedents to assess and reduce the risk of sudden cardiac death from hypertrophic cardiomyopathy.

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