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Independent relations of left ventricular structure with the 24-h urinary excretion of sodium and aldosterone
S82
Abstracts
expression on CD14+ monocytes were measured before and after one month treatment. TLR4 expression on CD14+ monocytes was quantified via flow-cytometry. Results: hsCRP and TLR4 expression on CD14+ monocytes in patients with ACS were higher than patients with stable angina (p < 0.05) and normal persons (p < 0.05). Serum hsCRP and TLR4 expression on CD4+ monocytes in patients with ACS were decreased after one month treatment with atorvastatin (p < 0.05). The effect of atorvastatin 40 mg/d on TLR4 expression was more effective than that of atorvastatin 10 mg/d (p < 0.05). Conclusions: Our study indicates that part of the anti-inflammatory effect of atorvastatin may be mediated by down-regulating the expression of TLR4. doi:10.1016/j.ijcard.2009.09.274 HT000815 Noninvasive assessment of cardiac structure and function in Apolipoprotein A-I amyloidosis (Leu75Pro) MASSIMO SALVETTI, MARIA LORENZA MUIESAN, ANNA PAINI, EUGENIA BELOTTI, CLAUDIA AGABITI ROSEI, CARLO AGGIUSTI, CRISTINA MONTEDURO, GINA GREGORINI, GIOVANNI CANCARINI, STEFANO PERLINI, ENRICO AGABITI ROSEI, FRANCESCO MARINO University of Brescia, Italy Background: Hereditary amyloidosis are late-onset autosomal dominant disorders characterized by amyloid deposition in various tissues. Among them, Apolipoprotein A-I amyloidosis (Leu75Pro) is a rare, autosomal dominant condition in which renal, hepatic, and testicular involvements have been demonstrated. Few data are available about cardiac involvement in this condition. The aim of the study was to evaluate cardiac structure and function in patients with Apolipoprotein A-I amyloidosis (APO A-I amyloidosis). Patients and methods: In 104 patients with Apolipoprotein A-I amyloidosis (Leu75Pro) (mean age 52 ± 16 years, 56 F, 57% hypertensives) and in 104 subjects matched for age, sex, body mass index (BMI) and clinic blood pressure (BP), left ventricular (LV) structure and function were evaluated by echocardiography (Mono-bidimensional + conventional and tissue Doppler analysis). Results: By definition no differences were observed for age, sex, BMI, BP and heart rate. LV mass index was significantly greater in patients with APO A-I amyloidosis than controls (35.6 ± 12.8 vs 32.7 ± 7.3 g/m2.7, p < 0.05). Relative wall thickness was similar in the two groups (0.32 ± 0.07 vs 0.30 ± 0.05, p = ns). The absolute value of mitral annular E velocity (Em) was significantly lower in patients with APO A-I amyloidosis (8.6 ± 3.4 vs 9.7 ± 2.2, p < 0.05), and the ratio of transmitral E velocity (E) to Em, (E/Em ratio) a sensitive index of LV filling pressure, was significantly greater (9.7 ± 4.2 vs 8.0 ± 2.1, p < 0.005). Ejection fraction, fractional shortening and midwall fractional shortening were significantly lower in amyloidosis as compared to controls (64.0 ± 7.0 vs 66.3 ± 5.9, p<0.05; 37.2 ±8.3 vs 40.2±7.4, p<0.005 and 19.2±3.8 vs 20.8± 3.0, p <0.001, respectively). Conclusion: In patients with Apolipoprotein A-I amyloidosis (Leu75Pro) a significant increase in LV mass associated with an impairment of systolic and diastolic function has been observed. These results, obtained in a wide sample of patients, may add significant information to the clinical features of this rare genetic disorder. doi:10.1016/j.ijcard.2009.09.275 HT000858 Independent relations of left ventricular structure with the 24-h urinary excretion of sodium and aldosterone Y. JINa, T. KUZNETSOVAa, M. MAILLARDc, T. RICHARTa,b, L. THIJSa, M. BOCHUDc, M.-C. HERREGODSd, M. BURNIERc, R. FAGARDa, J.A. STAESSENa,b
a
Studies Coordinating Centre, University of Leuven, Belgium Department of Epidemiology, Maastricht University, The Netherlands c The Division of Nephrology and Hypertension, University of Lausanne, Switzerland d Department of Cardiovascular Diseases, University of Leuven, Belgium b
Objective: Previous studies reported on the association of left ventricular mass index (LVMI) with urinary sodium or with circulating or urinary aldosterone. We investigated the independent associations of LVMI with the urinary excretion of both sodium and aldosterone. Design and method: We randomly recruited 317 untreated subjects from a White population (45.1% women; mean age 48.2 years). Measurements included echocardiographic left ventricular (LV) properties, the 24 h urinary excretion of sodium and aldosterone, plasma renin activity (PRA), and proximal (RNaprox) and distal (RNadist) renal sodium reabsorption, assessed from the endogenous lithium clearance. In multivariable-adjusted models, we expressed changes in LVMI per 1 SD increase in the explanatory variables, while accounting for sex, age, systolic blood pressure and the waist-to-hip ratio. Results: LVMI increased independently with the urinary excretion of both sodium (+2.48 g/m2; P=0.005) and aldosterone (+2.63 g/m2; P=0.004). Higher sodium excretion was associated with increased mean wall thickness (MWT: +0.126 mm, P=0.054), but with no change in LV end-diastolic diameter (LVID: +0.12 mm, P=0.64). In contrast, higher aldosterone excretion was associated with higher LVID (+0.54 mm; P=0.017), but with no change in MWT (+0.070 mm; P=0.28). Higher RNadist was associated with lower relative wall thickness (−0.81×10−2, P=0.017), because of opposite trends in LVID (+0.33 mm; P=0.13) and MWT (−0.130 mm; P=0.040). LVMI was not associated with PRA or RNaprox. Conclusions: LVMI independently increased with both urinary sodium and aldosterone excretion. Increased MWT explained the association of LVMI with urinary sodium and increased LVID the association of LVMI with urinary aldosterone. doi:10.1016/j.ijcard.2009.09.276
HT000860 Telomere length predicts left ventricular mass in a general population TATIANA KUZNETSOVA, VERYAN CODD, SCOTT BROUILETTE, LUTGARDE THIJS, YU JIN, TOM RICHART, JAN A. STAESSEN, NILESH J. SAMANI Hypertension Unit, University of Leuven, Belgium Department of Cardiovascular Sciences, University of Leicester, Leicester, UK Aims: Several experimental studies have implicated telomere dynamics in cardiomyocyte replication potential with shorter telomeres marking attenuated proliferation and increased apoptosis. We examined whether this translates into an impact of telomere length on left ventricular (LV) mass in the general population. Methods and results: In 334 participants (mean age, 46.5 years; 52.5% women) randomly selected from a Flemish population, we measured telomere length in circulating leukocytes by quantitative PCR and expressed it as the telomere/genomic DNA ratio (T/S). After a median interval of 7.4 years (IQR: 6.2 to 8.5 years) we measured LV mass by echocardiography. In multivariable-adjusted analyses accounting for sex, age, body weight and height, systolic blood pressure, and use of antihypertensive drugs, LV mass and LV mass index significantly increased with mean leukocyte telomere length in the entire population and especially in the sub-group of 198 normotensive subjects. For a 1-SD increment in the T/S ratio (approximately 0.75 kb), LV mass (mean 170 g) and mass index (mean 92 g/m2) increased by 5.25 g (P = 0.003) and 2.52 g/m2 (P = 0.009) in all subjects, and by 8.27 g (P = 0.0001) and 3.80 g/m2 (P = 0.001) in normotensive subjects. There were corresponding associations with LV wall thicknesses (P < 0.007), but not with LV internal diameter
Abstracts
expression on CD14+ monocytes were measured before and after one month treatment. TLR4 expression on CD14+ monocytes was quantified via flow-cytometry. Results: hsCRP and TLR4 expression on CD14+ monocytes in patients with ACS were higher than patients with stable angina (p < 0.05) and normal persons (p < 0.05). Serum hsCRP and TLR4 expression on CD4+ monocytes in patients with ACS were decreased after one month treatment with atorvastatin (p < 0.05). The effect of atorvastatin 40 mg/d on TLR4 expression was more effective than that of atorvastatin 10 mg/d (p < 0.05). Conclusions: Our study indicates that part of the anti-inflammatory effect of atorvastatin may be mediated by down-regulating the expression of TLR4. doi:10.1016/j.ijcard.2009.09.274 HT000815 Noninvasive assessment of cardiac structure and function in Apolipoprotein A-I amyloidosis (Leu75Pro) MASSIMO SALVETTI, MARIA LORENZA MUIESAN, ANNA PAINI, EUGENIA BELOTTI, CLAUDIA AGABITI ROSEI, CARLO AGGIUSTI, CRISTINA MONTEDURO, GINA GREGORINI, GIOVANNI CANCARINI, STEFANO PERLINI, ENRICO AGABITI ROSEI, FRANCESCO MARINO University of Brescia, Italy Background: Hereditary amyloidosis are late-onset autosomal dominant disorders characterized by amyloid deposition in various tissues. Among them, Apolipoprotein A-I amyloidosis (Leu75Pro) is a rare, autosomal dominant condition in which renal, hepatic, and testicular involvements have been demonstrated. Few data are available about cardiac involvement in this condition. The aim of the study was to evaluate cardiac structure and function in patients with Apolipoprotein A-I amyloidosis (APO A-I amyloidosis). Patients and methods: In 104 patients with Apolipoprotein A-I amyloidosis (Leu75Pro) (mean age 52 ± 16 years, 56 F, 57% hypertensives) and in 104 subjects matched for age, sex, body mass index (BMI) and clinic blood pressure (BP), left ventricular (LV) structure and function were evaluated by echocardiography (Mono-bidimensional + conventional and tissue Doppler analysis). Results: By definition no differences were observed for age, sex, BMI, BP and heart rate. LV mass index was significantly greater in patients with APO A-I amyloidosis than controls (35.6 ± 12.8 vs 32.7 ± 7.3 g/m2.7, p < 0.05). Relative wall thickness was similar in the two groups (0.32 ± 0.07 vs 0.30 ± 0.05, p = ns). The absolute value of mitral annular E velocity (Em) was significantly lower in patients with APO A-I amyloidosis (8.6 ± 3.4 vs 9.7 ± 2.2, p < 0.05), and the ratio of transmitral E velocity (E) to Em, (E/Em ratio) a sensitive index of LV filling pressure, was significantly greater (9.7 ± 4.2 vs 8.0 ± 2.1, p < 0.005). Ejection fraction, fractional shortening and midwall fractional shortening were significantly lower in amyloidosis as compared to controls (64.0 ± 7.0 vs 66.3 ± 5.9, p<0.05; 37.2 ±8.3 vs 40.2±7.4, p<0.005 and 19.2±3.8 vs 20.8± 3.0, p <0.001, respectively). Conclusion: In patients with Apolipoprotein A-I amyloidosis (Leu75Pro) a significant increase in LV mass associated with an impairment of systolic and diastolic function has been observed. These results, obtained in a wide sample of patients, may add significant information to the clinical features of this rare genetic disorder. doi:10.1016/j.ijcard.2009.09.275 HT000858 Independent relations of left ventricular structure with the 24-h urinary excretion of sodium and aldosterone Y. JINa, T. KUZNETSOVAa, M. MAILLARDc, T. RICHARTa,b, L. THIJSa, M. BOCHUDc, M.-C. HERREGODSd, M. BURNIERc, R. FAGARDa, J.A. STAESSENa,b
a
Studies Coordinating Centre, University of Leuven, Belgium Department of Epidemiology, Maastricht University, The Netherlands c The Division of Nephrology and Hypertension, University of Lausanne, Switzerland d Department of Cardiovascular Diseases, University of Leuven, Belgium b
Objective: Previous studies reported on the association of left ventricular mass index (LVMI) with urinary sodium or with circulating or urinary aldosterone. We investigated the independent associations of LVMI with the urinary excretion of both sodium and aldosterone. Design and method: We randomly recruited 317 untreated subjects from a White population (45.1% women; mean age 48.2 years). Measurements included echocardiographic left ventricular (LV) properties, the 24 h urinary excretion of sodium and aldosterone, plasma renin activity (PRA), and proximal (RNaprox) and distal (RNadist) renal sodium reabsorption, assessed from the endogenous lithium clearance. In multivariable-adjusted models, we expressed changes in LVMI per 1 SD increase in the explanatory variables, while accounting for sex, age, systolic blood pressure and the waist-to-hip ratio. Results: LVMI increased independently with the urinary excretion of both sodium (+2.48 g/m2; P=0.005) and aldosterone (+2.63 g/m2; P=0.004). Higher sodium excretion was associated with increased mean wall thickness (MWT: +0.126 mm, P=0.054), but with no change in LV end-diastolic diameter (LVID: +0.12 mm, P=0.64). In contrast, higher aldosterone excretion was associated with higher LVID (+0.54 mm; P=0.017), but with no change in MWT (+0.070 mm; P=0.28). Higher RNadist was associated with lower relative wall thickness (−0.81×10−2, P=0.017), because of opposite trends in LVID (+0.33 mm; P=0.13) and MWT (−0.130 mm; P=0.040). LVMI was not associated with PRA or RNaprox. Conclusions: LVMI independently increased with both urinary sodium and aldosterone excretion. Increased MWT explained the association of LVMI with urinary sodium and increased LVID the association of LVMI with urinary aldosterone. doi:10.1016/j.ijcard.2009.09.276
HT000860 Telomere length predicts left ventricular mass in a general population TATIANA KUZNETSOVA, VERYAN CODD, SCOTT BROUILETTE, LUTGARDE THIJS, YU JIN, TOM RICHART, JAN A. STAESSEN, NILESH J. SAMANI Hypertension Unit, University of Leuven, Belgium Department of Cardiovascular Sciences, University of Leicester, Leicester, UK Aims: Several experimental studies have implicated telomere dynamics in cardiomyocyte replication potential with shorter telomeres marking attenuated proliferation and increased apoptosis. We examined whether this translates into an impact of telomere length on left ventricular (LV) mass in the general population. Methods and results: In 334 participants (mean age, 46.5 years; 52.5% women) randomly selected from a Flemish population, we measured telomere length in circulating leukocytes by quantitative PCR and expressed it as the telomere/genomic DNA ratio (T/S). After a median interval of 7.4 years (IQR: 6.2 to 8.5 years) we measured LV mass by echocardiography. In multivariable-adjusted analyses accounting for sex, age, body weight and height, systolic blood pressure, and use of antihypertensive drugs, LV mass and LV mass index significantly increased with mean leukocyte telomere length in the entire population and especially in the sub-group of 198 normotensive subjects. For a 1-SD increment in the T/S ratio (approximately 0.75 kb), LV mass (mean 170 g) and mass index (mean 92 g/m2) increased by 5.25 g (P = 0.003) and 2.52 g/m2 (P = 0.009) in all subjects, and by 8.27 g (P = 0.0001) and 3.80 g/m2 (P = 0.001) in normotensive subjects. There were corresponding associations with LV wall thicknesses (P < 0.007), but not with LV internal diameter