Vagal enhancement due to subendocardial ischemia as a cause of abnormal blood pressure response in hypertrophic cardiomyopathy

Kawasaki, Tatsuya; Azuma, Akihiro; Kuribayashi, Toshiro; Akakabe, Yoshiki; Yamano, Michiyo; Miki, Shigeyuki; Sawada, Takahisa; Kamitani, Takeshi; Matsubara, Hiroaki; Sugihara, Hiroki

doi:10.1016/j.ijcard.2007.05.023

Cited by 16 publications

(17 citation statements)

References 31 publications

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“…Individuals with cardiomyopathies such as HCM are unable to demonstrate these changes and may exhibit a flat response or even a fall in blood pressure during exercise. 37 In some cases, particularly with families in which a definitive genetic mutation has already been identified, genetic testing may be considered. However, this can create challenges in terms of availability and expense, and test results generally may not be available for several weeks after ordering the exam.…”

Section: Other Imaging Modalitiesmentioning

confidence: 99%

Cardiac Imaging in Athletes

Khan

Safi

Wood

2016

Methodist DeBakey Cardiovascular Journal

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Athletic heart syndrome refers to the physiological and morphological changes that occur in a human heart after repetitive strenuous physical exercise. Examples of exercise-induced changes in the heart include increases in heart cavity dimensions, augmentation of cardiac output, and increases in heart muscle mass. These cardiac adaptations vary based on the type of exercise performed and are often referred to as sport-specific cardiac remodeling. The hemodynamic effects of endurance and strength training exercise lead to these adaptations. Any abnormalities in chamber dilatation and left ventricular function usually normalize with cessation of exercise. Athletic heart syndrome is rare and should be differentiated from pathologic conditions such as hypertrophic cardiomyopathy, left ventricular noncompaction, and arrhythmogenic right ventricular dysplasia when assessing a patient for athletic heart syndrome. This paper describes specific adaptations that occur in athletic heart syndrome and tools to distinguish between healthy alterations versus underlying pathology.

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Section: Other Imaging Modalitiesmentioning

confidence: 99%

Cardiac Imaging in Athletes

Khan

Safi

Wood

2016

Methodist DeBakey Cardiovascular Journal

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“…An abnormal blood pressure response to exercise in young HCM patients (<40 years old) is considered a risk factor for sudden cardiac death [16,22]. Proposed mechanisms include exaggerated peripheral vasodilation as well as decreased stroke volume with exercise [23,24]. Exercise testing can also be used to evaluate ischemia, which may be due to epicardial and/or microvascular coronary artery disease [25,26].…”

Section: Utility Of Exercise and Cardiopulmonary Testing In Hcm Patientsmentioning

confidence: 99%

Exercise in Hypertrophic Cardiomyopathy

Day

2009

J. of Cardiovasc. Trans. Res.

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The risk of sudden cardiac death (SCD) associated with vigorous athletic competition in individuals with hypertrophic cardiomyopathy (HCM) is well documented, and is the basis for recommended exclusion from competitive sports independent of other risk factors. Although SCD risk with recreational exercise is less well defined, published guidelines for participation in recreational sports, based on a consensus of expert opinion, offer a valuable framework for counseling patients. Exercise stress testing is an important diagnostic and prognostic tool in the evaluation of HCM patients, providing an objective measure of functional capacity, physiologic hemodynamic responses to stress, presence of ischemia, and provocable left ventricular outflow tract obstruction. The value of cardiopulmonary exercise testing in HCM is less well studied than in the heart failure population, but can be used to set a safe target for exercise intensity as part of an individualized exercise prescription. The long-term effects of exercise on HCM pathophysiology are largely theoretical at this stage. Potential harmful effects of fatiguing exercise include prolonged contractile dysfunction resulting from microvascular ischemia and energetic compromise. Conversely, several animal studies have shown that voluntary exercise prevents or reverses many pathologic features of HCM, including those related to apoptosis and energetics. Substantial evidence for health-promoting benefits of exercise in the general population, in addition to promising safety and efficacy data in patients with chronic heart failure, emphasizes the need to attain a reasonable balance between potential risks and benefits of aerobic fitness in individuals with HCM.

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“…The underlying pathophysiology that causes ABPR in patients with HC appears to be multifaceted and proposed mechanisms include: LV systolic dysfunction 15 with subsequent subendocardial myocardial ischemia 16,17 , altered baroreflex-mediated modulation of autonomic outflow to the heart and vasculature (possibly related to aforementioned subendocardial myocardial ischemia) 18 and subsequent altered vascular response to exercise (i.e. excessive fall in peripheral/systemic vascular resistance) 19 .…”

Section: Discussionmentioning

confidence: 99%

Relation of Pulse Pressure to Blood Pressure Response to Exercise in Patients With Hypertrophic Cardiomyopathy

Heffernan

Maron

Patvardhan

et al. 2011

The American Journal of Cardiology

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Almost one-third of patients with hypertrophic cardiomyopathy (HC) have an abnormal blood pressure response (ABPR) to exercise and this is associated with a greater risk of sudden cardiac death (SCD). In this study, we examined the association between steady (mean arterial pressure) and pulsatile (pulse pressure) blood pressure components as they relate to ABPR in patients with HC (n = 70). All patients completed a standard Bruce protocol during symptom limited stress testing with concurrent hemodynamic measurements. PP was significantly higher in HC patients with ABPR (n = 19) compared to HC patients with a normal BP response to exercise (p<0.05). According to binary logistic regression, resting PP was a significant predictor of ABPR in patients with HC (p<0.05). MAP was not significantly different between groups, nor was it a predictor of ABPR in HC. Those within the highest tertile of resting PP were 4.8 times more likely to have an ABPR compared to those within the lowest PP tertile (95% CI = 1.24 – 18.2, p<0.05). In conclusion, elevations in resting PP may identify HC individuals at higher risk for having an ABPR during exercise.

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Vagal enhancement due to subendocardial ischemia as a cause of abnormal blood pressure response in hypertrophic cardiomyopathy

Cited by 16 publications

References 31 publications

Cardiac Imaging in Athletes

Cardiac Imaging in Athletes

Exercise in Hypertrophic Cardiomyopathy

Relation of Pulse Pressure to Blood Pressure Response to Exercise in Patients With Hypertrophic Cardiomyopathy

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