Cardiac Hypertrophy – ABC CARDIOL

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My Approach to Echocardiography in Radiofrequency Ablation of Hypertrophic Obstructive Cardiomyopathy

Antonio Tito Paladino et al. Andrea de Andrade Vilela Jorge Eduardo Assef Bruno Pereira Valdigem

Introduction

Hypertrophic cardiomyopathy (HCM), an autosomal dominant genetic disease that affects one in 500 people, is considered the most common isolated form of hereditary heart disease. HCM is characterized by varying degrees of ventricular hypertrophy, myocardial fiber disarray, interstitial fibrosis, and microvascular disease in the absence of cardiac or systemic conditions to justify these findings.

Echocardiography, an invaluable tool for the diagnosis and follow-up of patients with HCM, is used to assess morphology, hemodynamic disorders, left ventricular (LV) function, and patient prognosis. It also has a fundamental role in cases of hypertrophic obstructive cardiomyopathy (HOCM) in the indication of invasive treatments. Radiofrequency ablation (RFA) is a possible treatment under study.

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Clinicoradiological Session

Case 5/2016 – Native Coarctation of the Aortic Arch, Relieved By Percutaneous Treatment in an Adult

Edmar Atik et al. Raul Arrieta

Complementary tests

Electrocardiogram showed sinus rhythm, signs of complete right bundle branch block wit QRS duration of 0.14”, and block of the anterior superior division of the left bundle branch (unchanged since neonatal aortic coarctation repair and interventricular communication). P axis: +20º, QRS axis: +250º, T axis: +35º.

Chest radiograph showed normal heart area and myocardial hypertrophy, and normal pulmonary vasculature.

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Artigo Original

Left ventricular hypertrophy of athletes: adaptative physiologic response of the heart

Nabil Ghorayeb et al. Michel Batlouni Ibraim M. F Pinto Giuseppe S Dioguardi

OBJECTIVE: To verify whether left ventricular hypertrophy (LVH) of elite competition athletes (marathoners) represents a purely physiological, adaptative process, or it may involve pathological aspects in its anatomical and functional characteristics. METHODS: From November 1999 to December 2000, consecutive samples from 30 under 50-year-old marathoners in full sportive activity, with previously documented LVH and absence of cardiopathy were selected. They were submitted to clinical exams, electrocardiogram, color Doppler echocardiogram and exercise treadmill test (ETT). Fifteen were assorted to be also submitted to ergoespirometric test and heart magnetic resonance imaging (MRI). RESULTS: In ETT, all of them showed good physical pulmonary capacity, with no evidences of ischemic response to exercise, symptoms or arrhythmias. In Doppler echocardiogram, values of diameter and diastolic thickness of LV posterior wall, interventricular septum, LV mass and left atrium diameter, were significantly higher when compared to non-athlete control group, with similar ages and anthropometric measurements. The mean of LV mass of athletes indexed to body surface (126 g/m2) was significantly greater than the one in control group (70 g/m2) (p<0.001). Magnetic resonance imaging (MRI) showed there was not impairment of contractile strength or LV performance, and values of end diastolic volume, end systolic volume and EF within limits of normality. On the other hand, average ventricular parietal mass, 162.93±17.90 g, and LV parietal thickness, 13.67±2.13 mm, at the end of diastole in athlete group, differed significantly from control group: 110±14.2 g (p=0.0001) and 8±0.9 mm, respectively (p=0.0001). The same happened to the thickness at the end of systole, which was 18.87±3.40 mm (control group: 10±1.80 mm, p=0.0001). CONCLUSION: Results allowed for concluding that LVH in marathoners in full sportive activity period, assessed by non-invasive methods, represents an adaptative response to intensive and prolonged physical training, with purely physiological characteristics.

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Artigo Original

Effects of the prolonged inhibition of the angiotensin-converting enzyme on the morphological and functional characteristics of left ventricular hypertrophy in rats with persistent pressure overload

Edson Antonio Bregagnollo et al. Katashi Okoshi Isamara Fernanda Bregagnollo Carlos Roberto Padovani … Marina P. Okoshi Antonio Carlos Cicogna

OBJECTIVE: To assess the effects of lisinopril (L) on mortality (M) rate and congestive heart failure (CHF), and the characteristics of geometrical myocardial remodeling and left ventricular function in rats with supravalvular aortic stenosis (SAS). METHODS: Some Wistar rats underwent SAS or the simulated surgery (CG, n=10). After 6 weeks, the animals were randomized to receive lisinopril (LG, n=30) or no treatment (SG, n=73) for 15 weeks. Cardiac remodeling was assessed in the sixth and 21st weeks after the surgical procedures through concomitant echocardiographic, hemodynamic, and morphological studies. RESULTS: The M were 53.9% and 16.7% in SG and LG, respectively; the incidence of CHF was 44.8% and 20%, in SG and LG, respectively, (P<0.05). At the end of the experiment, the values of LV systolic pressure in SG and LG were equivalent and significantly greater than those in CG;(P<0.05) and did not differ from those observed 6 weeks after the surgical procedures. The values of LV diastolic pressure in SG were greater than those in LG;(P<0.05), and both were greater than those in CG;(P0.05), and both were greater than those in SG;(P<0.05). Similar results were obtained with the values of the positive and negative first derivate of LV pressure. CONCLUSION: In rats with SAS, the treatment with L reduced M rate and ICC and had beneficial effects on geometrical myocardial remodeling and left ventricular function.

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Original Article

Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan

Antônio Carlos Avanza Jr et al. Lilian Mameri El Aouar José Geraldo Mill

OBJECTIVE: To compare the regression of left ventricular hypertrophy in patients with moderate hypertension treated with enalapril, losartan or a combination of the two drugs at lower doses. METHODS: Patients of both sexes with moderate hypertension confirmed by ambulatory monitoring of arte-rial blood pressure and with left ventricular hypertrophy on echocardiogram were assigned to three groups: enalapril (35 mg/day, n=15), losartan (175 mg/day, n=15) and enalapril+losartan (15 mg+100 mg/day, n=16). The patients received the drugs for 10 months. RESULTS: The three therapeutic regimens were equally effective in reducing blood pressure and left ventricular mass index (LVMI, g/m²): 141±3.9 to 123±3.6 in the enalapril group (p<0.05), from 147±3.8 to 133±2.8 in the losartan group (p<0.05), and from 146±3.0 to 116±4.0 in the enalapril+losartan group (p<0.05). However, the percent reduction of LVMI was significantly greater (p<0.01) in the enalapril+losartan group (20.5±5.0%) than in enalapril (12.4±3.2%) and the losartan (9.1±2.1%) groups. Normalization of LVMI was obtained in 10 out of the 16 patients who received enalapril+ losartan, in 6 out of the 15 patients who received only enalapril and in 4 out of the 15 patients treated with losartan. CONCLUSION: The combination of an angiotensin-converting enzyme inhibitor and an angiotensin II receptor antagonist (AT1 receptor antagonist) in patients produced an additional effect on the reduction of left ventricular hypertrophy. This finding may depend on a more complete inhibition of the cardiac renin-angiotensin.

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My Approach to Echocardiography in Radiofrequency Ablation of Hypertrophic Obstructive Cardiomyopathy

Introduction

Case 5/2016 – Native Coarctation of the Aortic Arch, Relieved By Percutaneous Treatment in an Adult

Complementary tests

Left ventricular hypertrophy of athletes: adaptative physiologic response of the heart

Effects of the prolonged inhibition of the angiotensin-converting enzyme on the morphological and functional characteristics of left ventricular hypertrophy in rats with persistent pressure overload

Reduction in left ventricular hypertrophy in hypertensive patients treated with enalapril, losartan or the combination of enalapril and losartan

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