Comparison of Coronary Vasodilator Reserve in Elite Rowing Athletes Versus Hypertrophic Cardiomyopathy

Radvan, J; Choudhury, Lubna; Sheridan, Desmond J.; Camici, Paolo G.

doi:10.1016/s0002-9149(97)00778-9

Cited by 37 publications

(31 citation statements)

References 12 publications

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“…They found that both resting and hyperemic (dipyridamole) MBF and CFR in the athletes and normal controls were comparable (Table). 41 Similar results were obtained in subsequent studies comparing MBF and CFR in elite athletes and control subjects, 42,43 suggesting that MBF and CFR are preserved in athletes with physiological LVH.…”

Section: Cmd In Physiological Lvhsupporting

confidence: 73%

From Left Ventricular Hypertrophy to Dysfunction and Failure

Lazzeroni

Rimoldi

Camici

2016

Circ J

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120

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Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. DCM is generally caused by viral/bacterial myocarditis, exposure to cardiotoxic substances or is a manifestation of a systemic disease. Before cell death and fibrotic repair occur, multiple factors contribute to contractile dysfunction, including abnormalities in sarcolemmal integrity, energy production, calcium handling and force transmission. 10 Both systolic and diastolic dysfunction worsen with time and EF is progressively reduced, with symptoms and signs of HF. Secondary LVHCardiomyocyte hypertrophy is the primary mechanism by which the heart counteracts a protracted increase in stress (or load) on the ventricular wall. 11 According to Laplace's law, 12 wall stress is directly related to LV cavity size and intracavitary pressure and inversely related to wall thickness. Thus, wall thickening will counteract, at least in part, the increased stress and oxygen demand caused by pressure or volume overload, although, in the long run, this compensatory mechanism may become maladaptive. On the other hand, several other nonhemodynamic factors, including activation of the adrenergic and renin-angiotensin-aldosterone (RAAS) systems, release of growth factors and cytokines, contribute to the development of LVH. 13,14 Pressure Overload In most cases, pressure overload manifests as arterial hypertension (AH) or aortic stenosis (AS).Hypertensive Heart The most common condition associated with an increase in cardiac afterload and wall stress is AH. 15 Approximately 20-60% of patients with uncomplicated AH have evidence of increased LVM on echocardiography. 16 LVM can increase from wall thickening, chamber dilatation or both. Wall thickening occurs more commonly in response to pressure overload whereas chamber dilation occurs more commonly in response to volume overload. Although LV wall thickness is more closely related to systemic diastolic blood pressure (concentric hypertrophy), reflecting pure pressure load caused by increased systemic vascular resistance...

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Section: Cmd In Physiological Lvhsupporting

confidence: 73%

From Left Ventricular Hypertrophy to Dysfunction and Failure

Lazzeroni

Rimoldi

Camici

2016

Circ J

Self Cite

120

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“…6 -8,11-13 However, studies in endurance athletes thus far provided data on morphology and function of LV myocardium 23,24 and size and dilating capacity of large coronary arteries, 24,25 while vasodilator capacity of coronary microcirculation was studied only in small series of young athletes without a control group of hypertensive patients with comparable LVH. 26,27 In this study, we took advantage of an integrated echocardiographic approach that allowed us to assess, in a noninvasive manner, resting coronary flow velocity together with the main determinants of myocardial oxygen demand, 16 -18 as well as the response of coronary flow velocity and epicardial vessel diameter to intravenous infusion of a vasodilator agent. 15,20 The main findings of the study are as follows: (1) in hypertensive LVH, the correlation between resting coronary flow velocity and determinants of myocardial oxygen demand is missing, while this relationship is preserved in physiological LVH; (2) maximal coronary vasodilation at the microcirculatory level is preserved in athletes with physiological LVH, while it is impaired in hypertensive LVH; (3) exercise training accompanied by physiological LVH is associated with a favorable remodeling and enhanced vasodilator capacity of the epicardial vessels; and (4) the effect of aging on coronary microcirculation is different between hypertensive subjects with LVH and athletes with physiological LVH.…”

Section: Discussionmentioning

confidence: 99%

Coronary Vasodilator Capacity and Epicardial Vessel Remodeling in Physiological and Hypertensive Hypertrophy

et al. 2000

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Abstract-The aim of this study was to compare resting coronary flow velocity, determinants of myocardial oxygen demand, and coronary vasodilator capacity in subjects with physiological, exercise-induced, and hypertensive left ventricular hypertrophy. Sixteen healthy sedentary men, 16 endurance athletes, and 16 hypertensive subjects (meanϮSEM for left ventricular mass index: 94.9Ϯ5.5, 184.6Ϯ8.4, 154.4Ϯ9.5 g/m 2 , respectively) were studied by transesophageal and transthoracic Doppler echocardiography. Coronary flow velocity in left anterior descending artery and cross-sectional area of left main artery were assessed at rest and during dipyridamole-induced vasodilation. Myocardial oxygen demand was estimated through rate-pressure product, left ventricular wall stress, and inotropic function. Coronary flow reserve and minimum coronary resistance were comparable to those of sedentary men in athletes (meanϮSEM: 3.23Ϯ0.16 versus 3.60Ϯ0.18 and 0.96Ϯ0.06 versus 1.04Ϯ0.04 mm Hg ⅐ s ⅐ cm Ϫ1 ), while in hypertensive subjects they were decreased and increased, respectively (meanϮSEM: 2.31Ϯ0.08 and 1.21Ϯ0.10 mm Hg ⅐ s ⅐ cm Ϫ1 ; PϽ0.05 for both). Resting flow velocity was directly related to rate-pressure product in sedentary men and athletes and also to wall stress in athletes, while these correlations were absent in hypertensives. Dilation of left main artery after dipyridamole was significantly higher in athletes than in sedentary men and hypertensive subjects (meanϮSEM for area change: 32.9Ϯ3.7% versus 12.8Ϯ2.5% and 6.4Ϯ3.3%; PϽ0.05 and 0.01). These data indicate that vasodilator capacity of coronary microcirculation is not impaired in athletes with physiological hypertrophy, in contrast to hypertensive patients. The relationship between resting flow velocity and determinants of oxygen demand is preserved in physiological hypertrophy but missing in hypertensive hypertrophy. Furthermore, the vasodilator capacity of coronary macrocirculation is also enhanced in exercise-trained subjects. Key Words: hypertrophy, left ventricular Ⅲ circulation Ⅲ exercise Ⅲ aging L eft ventricular hypertrophy (LVH) represents an adaptive mechanism by which the heart normalizes wall stress and preserves left ventricular (LV) function. Both systemic hypertension and chronic exercise training may induce LVH. While hypertensive LVH represents a risk factor for cardiovascular morbidity and mortality 1 and is associated with an impairment in coronary vasodilator capacity, 2,3 chronic exercise training is supposed to improve cardiovascular capacity and to reduce morbidity and mortality. 4,5 Experimental studies suggest an exercise-induced protective adaptation in coronary circulation, which may include both structural changes 6,7 and changes in vasomotor responses. 8 -10 It was demonstrated that in normotensive animals, such as rat, 11,12 dog, 13 and swine, 7 chronic exercise training results in an improvement of coronary vasodilator reserve. By contrast, studies comparing coronary vasodilator capacity in hypertensive patients with LVH and physicall...

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“…* P < 0.05 endurance trained vs. controls. coronary vasodilator capacity that is seen in pathological hypertrophy due to cardiomyopathy (Radvan et al 1997) or hypertension in humans (Kozakova et al 2000) or animals (Tomanek, 1990;Tomanek & Torry, 1994). The conclusion is that there is expansion of the resistance vasculature commensurate with cardiac hypertrophy through growth in numbers of smaller arterial vessels, although there are surprisingly few rigorous morphometric studies of all size classes of coronary resistance vessels in response to exercise training.…”

Section: Figurementioning

confidence: 99%

Physiological Society Symposium – the Athlete's Heart

Brown

2003

Experimental Physiology

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In this review the evidence for structural adaptations of the coronary circulation in the healthy adult heart in response to exercise and training is examined. Previously, it was thought that expansion of the coronary arteries and resistance vasculature occurred without angiogenesis. Detailed studies of the time course of coronary vascular remodelling now reveal that capillary proliferation is an integral response to exercise training, but is disguised by concurrent transformation of capillaries into arterioles by ‘arteriolarization’. Increases in numbers of small arterioles < 30 µm in diameter are accompanied by expansion in calibre of resistance and large coronary arteries. Stimuli related to increases in blood flow ‐ shear stress and wall tension ‐ and to mechanical deformation of the myocardium ‐ stretch and compression ‐ provide the main impetus for coronary vascular remodelling. Despite the technical difficulties of measuring such parameters in the heart in vivo, intervention studies using specific exercise components such as vasodilator, inotropic and chronotropic manipulations have allowed some insight into the differential regional effects of haemodynamic factors throughout the vascular tree. It remains to establish more clearly the involvement of mediators such as nitric oxide and growth factors in the temporal relationship to endothelial and smooth muscle growth and proliferation so that the endogenous attributes of exercise can be exploited for therapeutic purposes.

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Comparison of Coronary Vasodilator Reserve in Elite Rowing Athletes Versus Hypertrophic Cardiomyopathy

Cited by 37 publications

References 12 publications

From Left Ventricular Hypertrophy to Dysfunction and Failure

From Left Ventricular Hypertrophy to Dysfunction and Failure

Coronary Vasodilator Capacity and Epicardial Vessel Remodeling in Physiological and Hypertensive Hypertrophy

Physiological Society Symposium – the Athlete's Heart

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