Hypertrophic cardiomyopathy (HCM) is the most frequent cardiac disease with genetic substrate, affecting about 0.2-0.5% of the population. While most of the patients with HCM have a relatively good prognosis, some are at increased risk of adverse events. Identifying such patients at risk is important for optimal treatment and follow-up. While clinical and electrocardiographic information plays an important role, echocardiography remains the cornerstone in assessing patients with HCM. In this review, we discuss the role of echocardiography in diagnosing HCM, the key features that differentiate HCM from other diseases and the use of echocardiography for risk stratification in this setting (risk of sudden cardiac death, heart failure, atrial fibrillation and stroke). The use of modern echocardiographic techniques (deformation imaging, 3D echocardiography) refines the diagnosis and prognostic assessment of patients with HCM. The echocardiographic data need to be integrated with clinical data and other information, including cardiac magnetic resonance, especially in challenging cases or when there is incomplete information, for the optimal management of these patients.
Aims To assess the carotid mechanical properties in patients with hypertrophic cardiomyopathy and the relation between arterial stiffness and left ventricular function in this setting. Methods and results We have prospectively enrolled 71 patients (52 ± 16 years, 34 men) with hypertrophic cardiomyopathy, divided into two groups depending on the presence (46 patients) or absence (25 patients) of cardiovascular risk factors associated with increased arterial stiffness. Twenty-five normal subjects similar by age and gender with hypertrophic cardiomyopathy patients without risk factors formed the control group. A comprehensive echocardiography was performed in all subjects. Carotid arterial stiffness index (β index), pressure–strain elastic modulus, arterial compliance, and pulse wave velocity were also obtained using an echo-tracking system. β index, pulse wave velocity, and pressure–strain elastic modulus were significantly higher in hypertrophic cardiomyopathy patients without risk factors compared to controls. After linear regression analysis, the increase in carotid β index was independently correlated with the presence of hypertrophic cardiomyopathy [beta = 0.49, 95% confidence interval (CI) = 1.04–3.02; P < 0.001]. In the entire hypertrophic cardiomyopathy population arterial stiffness parameters correlated with age, gender, hypertension degree, presence of hypercholesterolaemia, and the E/e′ ratio. In multivariable analysis, β index (beta = 0.36, 95% CI = 0.32–1.25; P = 0.001), global left ventricular longitudinal strain, and the presence of left ventricular outflow tract obstruction were independently correlated with the E/e′ ratio. Conclusion In patients with hypertrophic cardiomyopathy arterial stiffness is increased independently of age or presence of cardiovascular risk factors. Carotid artery stiffness is independently related to left ventricular filling pressure, increased arterial stiffness representing a possible marker of a more severe phenotype.
Hypertensive patients had smaller indexed aortic root dimensions than normal subjects but they had heigher prevalence of trivial-mild aortic regurgitation in contrast to normotensives who had aortic regurgitation combined with larger aortic diameters.
Funding Acknowledgements Type of funding sources: None. Background Although earlier publications suggested a more benign clinical course for patients (pts) with apical hypertrophic cardiomyopathy (ApHCM), recent studies report increased morbidity and mortality, comparable to the prognosis of other HCM variants. Moreover, information regarding cardiac remodelling and its relationship with symptoms in pts with ApHCM is scarce. The aim of our study was to assess left ventricular (LV), right ventricular (RV) and left atrial (LA) remodelling in pts with ApHCM in comparison with non-apical variants of HCM (nonApHCM), and the impact of cardiac remodelling on heart failure symptoms. Methods One hundred fifty-one consecutive pts with HCM (52 ± 16 yrs, 47% men) in sinus rhythm and with preserved LV ejection fraction (16 pts with ApHCM and 135 pts with nonApHCM), were prospectively enrolled. Comprehensive echocardiography was performed in all, including the measurement of maximal LV wall thickness (LVWT), RV free wall thickness (RVWT) and maximal LA volume indexed to body surface area (LAVi). Global LV strain (ɛ), RVɛ, LAɛ and end-diastolic LA strain rate (ASr) were measured using speckle-tracking echocardiography (STE). The ratio of E to average e’ was used to estimate LV filling pressure. The degree of mitral regurgitation (1/2/3) has also been assessed. Heart failure symptoms were defined according to the New York Heart Association (NYHA) classification. Results Forty-eight pts in nonApHCM group had intraventricular obstruction. There were no significant differences between pts with and without ApHCM regarding: age (58 ± 20 vs 52 ± 16 yrs), gender distribution, RVWT, LVɛ (-14.9 ± 2.7 vs -13.9 ± 3.5 %), RVɛ (-19.6 ± 3.6 vs -10.0 ± 5.0%), LAɛ (19.2 ± 5.8 vs 16.4 ± 7.1%)(p > 0.05 for all). Pts with ApHCM had lower values for LVWT (17.2 ± 1.9 vs 21.4 ± 5.2 mm, p = 0.002), E/e’ (12.0 ± 5.8 vs 17.6 ± 8.5, p = 0.02) and LAVi (48 ± 16 vs 61 ± 25, p = 0.03) compared to pts with nonApHCM. Pts with ApHCM had slightly better LA contractile function as assessed by ASr (-1.23 ± 0.50 vs -0.97 ± 0.49 sec-1, p = 0.05). Mitral regurgitation was more often severe in nonApHCM pts (56/42/31 vs 10/4/0, p < 0.001). There was no significant difference between the percentage of symptomatic pts (NYHA class ≥2) in ApHCM vs nonApHCM group (p = 0.3). In the ApHCM group, symptomatic pts had significantly lower ASr compared to asymptomatic pts (-0.98 ± 0.35 vs -1.61 ± 0.46 sec-1, p = 0.01). Conclusions Despite of lower LVWT values, less severe MR and no obstruction, pts with apical HCM have similar prevalence of heart failure symptoms, and similar LV, RV and LA dysfunction compared to pts with non-apical HCM. Symptomatic pts with apical HCM have worse LA contractile function compared to asymptomatic pts.
BackgroundPatients with hypertrophic cardiomyopathy (HCM) have an increased prevalence of atrial fibrillation (AF) compared to the general population, and left atrium (LA) remodeling is strongly correlated with the risk of AF. This prospective, monocentric study aimed to assess the role of LA electrocardiographic and echocardiographic (structural and functional) parameters in predicting the risk for incident AF in patients with HCM.Methods and ResultsThe study population consisted of 126 HCM patients in sinus rhythm (52.6 ± 16.2 years, 54 men), 118 of them without documented AF. During a median follow-up of 56 (7–124) months, 39 (30.9%) developed a new episode of AF. Multivariable analysis showed that LA booster pump function (assessed by ASr, HR = 4.24, CI = 1.84–9.75, and p = 0.038) and electrical dispersion (assessed by P wave dispersion – Pd, HR = 1.044, CI = 1.029–1.058, and p = 0.001), and not structural parameters (LA diameter, LA volume) were independent predictors of incident AF. Seventy-two patients had a LA diameter < 45 mm, and 16 of them (22.2%) had an AF episode during follow-up. In this subgroup, only Pd emerged as an independent predictor for incident AF (HR = 1.105, CI = 1.059–1.154, and p = 0.002), with good accuracy (AUC = 0.89).ConclusionLeft atrium booster pump function (ASr) and electrical dispersion (Pd) are related to the risk of incident AF in HCM patients. These parameters can provide further stratification of the risk for AF in this setting, including in patients considered at lower risk for AF based on the conventional assessment of LA size.
Background The clinical course of hypertrophic cardiomyopathy (HCM) is heterogeneous and the development of heart failure (HF) is difficult to predict. Exercise echocardiography can provide information about mechanisms involved in the occurrence of HF symptoms: development of intraventricular obstruction, increase in mitral regurgitation (MR) severity, impaired left ventricular (LV) and left atrial (LA) function. Purpose To analyse the changes in LV and LA function during exercise and to identify the main correlates of exercise capacity in patients (pts) with HCM, in sinus rhythm and with normal LV ejection fraction. Methods We have prospectively enrolled 32 pts (48±17 years, 15 men) with HCM and no obstruction at rest. A symptom limited exercise echocardiogram was performed in all pts using a table ergometer. Maximum LV wall thickness (LVWT), indexed left atrial volume (LAVi), septal E', E/septal E' ratio, were measured at rest (r) and during exercise (e). Global longitudinal LV strain (GLS) and LA strain (LAɛ) were assessed by speckle tracking echocardiography at rest and during exercise. The peak LV outflow tract gradient, systolic pulmonary artery pressure (PAP), and MR degree were recorded at rest and during exercise. Exercise-related symptoms, peak exercise heart rate (HR) and exercise capacity calculated in metabolic equivalents (METs) were also recorded. Results The mean value of achieved METs was 5.9±1.4, the peak HR was 124±25 bpm, representing 72±12% of maximal HR, during a mean of 8.5±2.5 minutes of exercise. Thirteen pts developed LV gradients >30 mmHg. Fifteen pts were asymptomatic, while 17 pts reported dyspnea during exercise. There were no significant differences between pts with and without symptoms regarding: age, rE', rE/E', rGLS, rLAɛ, rMR, rPAP, LAVi, eE/e', eGLS, eMR, ePAP (p>0.05 for all). Symptomatic pts had lower values for eE' (p=0.01), eLAɛ (p=0.03) and tended to have higher values for LVWT (p=0.06) and a higher prevalence of eLV outflow tract obstruction (p=0.13) compared to asymptomatic pts. In symptomatic group of pts, E' (p=0.004), PAP (p<0.001) and GLS (p=0.04) significantly increased and LAɛ tended to decrease (p=0.18) during exercise. Age (r=−0.44, p=0.01), rE' (r=0.40, p=0.02), eE' (r=0.46, p=0.01), ePAP (r=−0.35, p=0.04) and LVWT (r=−0.32, p=0.07) significantly correlated with achieved METs in HCM pts overall. In multivariate analysis, eE' (β=0.60, 95% CI 0.122 to 0.009, p=0.003) was the only parameter independently correlated with exercise capacity (expressed in METs). Conclusions Symptomatic pts had a worse LV diastolic function (as expressed by E') and a severe LA longitudinal dysfunction (as expressed by LAɛ) during exercise. E' during exercise was the only parameter independently correlated with exercise capacity in pts with HCM. These suggest that a detailed analysis of LV and LA function during exercise could provide additional information to predict the occurrence of HF in HCM pts.
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