Abstract 3391: Prevalence Of Hypertrophic Cardiomyopathy In Elite Athletes

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Sandeep Basavarajaiah ◽  
Mathew Wilson ◽  
Agnes Chlebinska ◽  
Arash Yavari ◽  
Gordon Jackson ◽  
...  

Objectives: The prevalence of HCM in the general population is estimated to be around 1 in 500. The exact prevalence of HCM in athletes has never been reported and has important implications with regards to potential future national pre-participation screening programme in countries such as United Kingdom, where currently there is no such programme for junior athletes. Methods: Between 1996 and 2006, 3500 asymptomatic and normotensive elite athletes (70% males) aged between 14–35 years (mean: 20.5±5.80) and a mean body surface area of 1.86±0.16 m 2 (range1.36–2.29) underwent 12-lead EKG and 2D-echocardiography. Cardiac dimensions and function were measured using conventional methods. Results: Of the 3500 athletes, 53 (2%) had maximal left ventricular wall thickness (LVWTd) > 12 mm (mean: 13.6 ± 0.9, range: 13–16). All 53 were male athletes and all except 3 of them had associated dilated LV cavity (58.5 ± 5.14 mm, range 52– 65) implying physiological left ventricular hypertrophy (LVH). This was also supported by normal indices of diastolic function and absence of family history of HCM or sudden cardiac death (SCD). However, there were 3 athletes with LVWT > 12mm who had a relatively non-dilated LV cavity (range:45– 46) and bizarre EKG changes (deep T-wave inversion) that that raised the suspicion of HCM. But none of them exhibited any other phenotypic feature of HCM on further testing with 48-hour EKG recording, cardiopulmonary exercise testing and assessment of their first-degree family members. Only one of the 3 athletes agreed to detrain for 12-weeks, which resulted in regression of LVH and complete resolution of EKG changes. Conclusion: In our study, only 3 athletes had echocardiographic findings that could have been consisted with the diagnosis of HCM but further investigations failed to support the diagnosis. These results indicate that the prevalence of HCM in highly trained athletes is extremely rare. The structural and functional changes associated with HCM precludes generation of large amounts of cardiac output that are required during exercise selecting out most of these individuals from competitive sports. Our findings also questions the validity of previous data which proposes that HCM is the commonest cause of exercise related SCD in young athletes.

2005 ◽  
Vol 289 (4) ◽  
pp. H1408-H1416 ◽  
Author(s):  
Andrew Fenning ◽  
Glenn Harrison ◽  
Roselyn Rose’meyer ◽  
Andrew Hoey ◽  
Lindsay Brown

Nitric oxide (NO) is essential for normal function of the cardiovascular system. This study has determined whether chronic administration of l-arginine, the biological precursor of NO, attenuates the development of structural and functional changes in hearts and blood vessels of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Uninephrectomized rats treated with DOCA (25 mg every 4th day sc) and 1% NaCl in the drinking water for 4 wk were treated with l-arginine (5% in food, 3.4 ± 0.3 g·kg body wt−1·day−1). Changes in cardiovascular structure and function were determined by echocardiography, microelectrode studies, histology, and studies in isolated hearts and thoracic aortic rings. DOCA-salt hypertensive rats developed hypertension, left ventricular hypertrophy with increased left ventricular wall thickness and decreased ventricular internal diameter, increased inflammatory cell infiltration, increased ventricular interstitial and perivascular collagen deposition, increased passive diastolic stiffness, prolonged action potential duration, increased oxidative stress, and inability to increase purine efflux in response to an increased workload. l-Arginine markedly attenuated or prevented these changes and also normalized the reduced efficacy of norepinephrine and acetylcholine in isolated thoracic aortic rings of DOCA-salt hypertensive rats. This study suggests that a functional NO deficit in blood vessels and heart due to decreased NO synthase activity or increased release of reactive oxygen species such as superoxide may be a key change initiating many aspects of the cardiovascular impairment observed in DOCA-salt hypertensive rats. These changes can be prevented or attenuated by administration of l-arginine.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Borrelli ◽  
P Sciarrone ◽  
F Gentile ◽  
N Ghionzoli ◽  
G Mirizzi ◽  
...  

Abstract Background Central apneas (CA) and obstructive apneas (OA) are highly prevalent in heart failure (HF) both with reduced and preserved systolic function. However, a comprehensive evaluation of apnea prevalence across HF according to ejection fraction (i.e HF with patients with reduced, mid-range and preserved ejection fraction- HFrEf, HFmrEF and HFpEF, respectively) throughout the 24 hours has never been done before. Materials and methods 700 HF patients were prospectively enrolled and then divided according to left ventricular EF (408 HFrEF, 117 HFmrEF, 175 HFpEF). All patients underwent a thorough evaluation including: 2D echocardiography; 24-h Holter-ECG monitoring; cardiopulmonary exercise testing; neuro-hormonal assessment and 24-h cardiorespiratory monitoring. Results In the whole population, prevalence of normal breathing (NB), CA and OA at daytime was 40%, 51%, and 9%, respectively, while at nighttime 15%, 55%, and 30%, respectively. When stratified according to left ventricular EF, CA prevalence decreased from HFrEF to HFmrEF and HFpEF: (daytime CA: 57% vs. 43% vs. 42%, respectively, p=0.001; nighttime CA: 66% vs. 48% vs. 34%, respectively, p<0.0001), while OA prevalence increased (daytime OA: 5% vs. 8% vs. 18%, respectively, p<0.0001; nighttime OA: 20 vs. 29 vs. 53%, respectively, p<0.0001). When assessing moderte-severe apneas, defined with an apnea/hypopnea index >15 events/hour, prevalence of CA was again higher in HFrEF than HFmrEF and HFpEF both at daytime (daytime moderate-severe CA: 28% vs. 19% and 23%, respectively, p<0.05) and at nighttime (nighttime moderate-severe CA: 50% vs. 39% and 28%, respectively, p<0.05). Conversely, moderate-severe OA decreased from HFrEF to HFmrEF to HFpEF both at daytime (daytime moderate-severe OA: 1% vs. 3% and 8%, respectively, p<0.05) and nighttime (noghttime moderate-severe OA: 10% vs. 11% and 30%, respectively, p<0.05). Conclusions Daytime and nighttime apneas, both central and obstructive in nature, are highly prevalent in HF regardless of EF. Across the whole spectrum of HF, CA prevalence increases and OA decreases as left ventricular systolic dysfunction progresses, both during daytime and nighttime. Funding Acknowledgement Type of funding source: None


1991 ◽  
Vol 70 (6) ◽  
pp. 2650-2655 ◽  
Author(s):  
D. C. McKenzie ◽  
L. S. Goodman ◽  
C. Nath ◽  
B. Davidson ◽  
G. O. Matheson ◽  
...  

Six male Quechua Indians (34.0 +/- 1.1 yr, 159.5 +/- 2.1 cm, 60.5 +/- 1.6 kg), life-long residents of La Raya, Peru (4,350-m altitude with an average barometric pressure of 460 Torr), were studied using noninvasive methods to determine the structural and functional changes in the cardiovascular system in response to a 6-wk deacclimation period at sea level. Cardiac output, stroke volume, and left ventricular ejection fractions were determined using radionuclide angiographic techniques at rest and during exercise on a cycle ergometer at 40, 60, and 90% of a previously determined maximal O2 consumption. Subjects at rest were subjected to two-dimensional and M-mode echocardiograms and a standard 12-lead electrocardiogram. Hemoglobin and hematocrit were measured on arrival at sea level by use of a Coulter Stacker S+ analyzer. After a 6-wk deacclimation period, all variables were remeasured using the identical methodology. Hemoglobin values decreased significantly over the deacclimation period (15.7 +/- 1.1 to 13.5 +/- 1.2 g/dl; P less than 0.01). The results indicate that the removal of these high-altitude-adapted natives from 4,300 m to sea level for 6 wk results in only minor changes to the cardiac structure and function as measured by these noninvasive techniques.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Sandeep Basavarajaiah ◽  
Lorna Carby ◽  
Arash Yavari ◽  
Anupama Nandagudi ◽  
Gordon Jackson ◽  
...  

Objectives: The upper limits of physiologic increase in the left ventricular (LV) dimensions for the purposes of differentiation from cardiomyopathies are well established in Caucasian athletes. However, there are few data regarding the physiologic LV remodelling in black athletes (BA) in whom deaths from cardiomyopathies are more prevalent. Methods: Between 2005 and 2006, 200 asymptomatic and normotensive black (African/AfroCaribbean) male athletes (mean age: 20.5 ± 5.80; range 14 –35 years and a mean BSA: 1.94 ± 0.16 m 2 ; range1.36 –2.29) underwent 12-lead EKG and 2-D echocardiography. The results were compared to those of 100 black controls (BC) and 200 highly trained white male athletes matched for age, size, sport and training programs. None of them had a family history of cardiomyopathy. Cardiac dimensions and function were measured in accordance using conventional methods. Results: The LV dimensions of black athletes (BA) compared with black controls (BC) and WA are shown below Data expressed as mean ± standard deviation (range) LVWTd- left ventricular wall thickness in end diastole LVIDd- left ventricular internal dimensions in end diastole Both BA and WA had a greater LV dimensions than BC. Black athletes had greater LVWT than WA amounting to a difference of 11%. In absolute terms, 40 (20%) BA had a LVWT > 12 mm compared with 12 (6%) WA. There were no significant differences in the LV cavity size or indices of diastolic function between BA and WA. All BA with a LVWT > 12 mm had an enlarged LV cavity size and normal indices of diastolic function indicating physiologic left ventricular hypertrophy (LVH) rather than hypertrophic cardiomyopathy (HCM). Conclusion: •Black athletes develop modest increase in the LV dimensions as compared to BC. •The magnitude of LVH in BA is significantly greater than in WA. •More BA have absolute LVWT values in the region compatible with morphologically mild HCM. •Our study calls for a separate physiologic upper limits for LV dimensions in BA.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Thida tabucanon ◽  
Timothy Engelman ◽  
Sanjeeb S Bhattacharya ◽  
J Emanuel Finet ◽  
Wai Hong W Tang

Introduction: Microalbuminuria can be a presentation of microvascular complication in diabetes mellitus (DM). Hypothesis: Microalbuminuria is associated with impaired exercise performance in chronic HF with DM patients. Methods: We retrospectively analyzed a cardiopulmonary exercise testing (CPET) database in 255 chronic HF patients with DM that had urine microalbumin test between December 2012 and September 2019. Demographic data and CPET parameters were compared between the patients who had and had not microalbuminuria which was defined by microalbumin/creatinine ratio ≥ 30 mg/g. Peak oxygen consumption (peak VO 2 ) ≤ 14 ml/kg/min and ≤ 12 ml/kg/min if had history of beta-blocker uses were classified as low peak VO 2 and used in multivariable analysis. Results: There were a total 92 patients (36.1%) that had microalbuminuria. Mean age was not significant different between the patients with and without microalbuminuria (57.7 vs 59.4 years, p = 0.26). The patients with microalbuminuria had lower body mass index (BMI; 30.8 vs. 32.7 kg/m 2 , p = 0.014) and had more history of beta-blocker (BB) uses (81.5% vs. 69.3%, p = 0.038), no significant different in other medication uses. Left ventricular ejection fraction (LVEF) was significant lower in patients with microalbuminuria (35.8% vs. 41.5%, p = 0.028). The patients with microalbuminuria had significant higher prevalence of low peak VO 2 (45.7% vs. 30.1%, p = 0.015) and lower peak stroke work (VO 2 /HR; 11.5 vs. 12.8 ml/ beat, p = 0.008). No significant different in ventricular efficiency slope (VE/VCO 2 ; 37.1 vs. 35.4, p = 0.094), Multivariable analysis showed that proteinuria was independently associated with low peak VO 2 after adjusted for age, sex, BMI LVEF, history of BB uses, VE/VCO 2 and HR at peak VO 2 , (odds ratio = 3.83, p < 0.001). Conclusions: Microalbuminuria was independently associated with low peak oxygen consumption in chronic HF with DM patients.


Open Heart ◽  
2020 ◽  
Vol 7 (2) ◽  
pp. e001273
Author(s):  
Odayme Quesada ◽  
Ki Park ◽  
Janet Wei ◽  
Eileen Handberg ◽  
Chrisandra Shufelt ◽  
...  

AimsHypertensive disorders of pregnancy (HDP) predict future cardiovascular events. We aim to investigate relations between HDP history and subsequent hypertension (HTN), myocardial structure and function, and late gadolinium enhancement (LGE) scar.Methods and resultsWe evaluated a prospective cohort of women with suspected ischaemia with no obstructive coronary artery disease (INOCA) who underwent stress/rest cardiac magnetic resonance imaging (cMRI) with LGE in the Women’s Ischemia Syndrome Evaluation-Coronary Vascular Dysfunction study. Self-reported history of pregnancy and HDP (gestational HTN, pre-eclampsia, toxaemia and eclampsia) were collected at enrollment. In our cohort of 346, 20% of women report a history of HDP. HDP history was associated with 3.2-fold increased odds of HTN. Women with a history of both HDP and HTN had higher cMRI measured left ventricular (LV) mass compared with women with HDP only (99.4±2.6 g vs 87.7±3.2 g, p=0.02). While we found a similar frequency of LGE scar, we observed a trend towards increased LGE scar size (5.1±3.4 g vs 8.0±3.4 g, p=0.09) among the women with HDP history compared to women without.ConclusionIn a high-risk cohort of women with suspected INOCA, 20% had a history of HDP. Women with HDP history were more likely to develop HTN. Our study demonstrates higher LV mass in women with HDP and concomitant HTN. Although the presence of LGE scar was not different in women with and without HDP history, we observed a trend towards larger scar size in women with HDP. Future studies are needed to better assess the relationship of HDP and cardiac morphology and LGE scarring in a larger cohort of women.


2018 ◽  
Vol 315 (6) ◽  
pp. R1232-R1241 ◽  
Author(s):  
Loren P. Thompson ◽  
Ling Chen ◽  
Brian M. Polster ◽  
Gerard Pinkas ◽  
Hong Song

Adverse intrauterine conditions cause fetal growth restriction and increase the risk of adult cardiovascular disease. We hypothesize that intrauterine hypoxia impairs fetal heart function, is sustained after birth, and manifests as both cardiac and mitochondrial dysfunction in offspring guinea pigs (GPs). Pregnant GPs were exposed to 10.5% O2 (HPX) at 50 days of gestation (full term = 65 days) or normoxia (NMX) for the duration of the pregnancy. Pups were allowed to deliver vaginally and raised in a NMX environment. At 90 days of age, mean arterial pressure (MAP) was measured in anesthetized GPs. NMX and prenatally HPX offspring underwent echocardiographic imaging for in vivo measurement of left ventricular cardiac morphology and function, and O2 consumption rates and complex IV enzyme activity were measured from isolated cardiomyocytes and mitochondria, respectively. Prenatal HPX increased ( P < 0.01) MAP (52.3 ± 1.3 and 58.4 ± 1.1 mmHg in NMX and HPX, respectively) and decreased ( P < 0.05) stroke volume (439.8 ± 54.5 and 289.4 ± 15.8 μl in NMX and HPX, respectively), cardiac output (94.4 ± 11.2 and 67.3 ± 3.8 ml/min in NMX and HPX, respectively), ejection fraction, and fractional shortening in male, but not female, GPs. HPX had no effect on left ventricular wall thickness or end-diastolic volume in either sex. HPX reduced mitochondrial maximal respiration and respiratory reserve capacity and complex IV activity rates in hearts of male, but not female, GPs. Prenatal HPX is a programming stimulus that increases MAP and decreases cardiac and mitochondrial function in male offspring. Sex-related differences in the contractile and mitochondrial responses suggest that female GPs are protected from cardiovascular programming of prenatal HPX.


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