In the Journals

NASH linked to early markers of hypertrophy

A retrospective study revealed a link between nonalcoholic steatohepatitis and changes in myocardial structure as well as increased left atrial volume and left ventricular mass.

“We found that NASH was strongly associated with markers of diastolic dysfunction and also with ventricular wall thickening, indicative of early hypertrophy,” Tracey G. Simon, MD, from the Massachusetts General Hospital and Harvard Medical School, Boston, and colleagues wrote. “Such findings carry important clinical implications, as diastolic dysfunction is a well-described predictor of future [heart failure] risk within the general population.”

Between Jan. 1, 2005, and Aug. 1, 2016, 78 patients underwent elective bariatric surgery and transthoracic echocardiography within 12 months of surgery. Sixty-five of these patients met inclusion criteria. Median age was 47 years (range, 35-56.5) and etiologies included normal hepatic histology (n = 18), steatosis without ballooning or lobular inflammation (n = 33) and NASH defined by the presence of steatosis with ballooning or lobular inflammation (n = 14).

Compared with other patients in the study, those with NASH had higher median BMI (45 kg/m2 vs. 43.7 kg/m2; P = .003), were more likely to have diabetes (45% vs. 29%; P = .003), more likely to have a family history of type 1 coronary disease (67% vs. 19%; P = .016), and had higher median left atrial volume (28.6 mL/m2 vs. 24.8 mL/m2; P < .0001) and left ventricular mass (82.6 g/m2 vs. 78.6 g/m2; P < .0001).

After adjusting for age, sex, diabetes, hypertension, and BMI, the researchers found that NASH remained associated with increased left ventricular mass for height (beta1 = 7.16; P = 0.001) and left atrial volume for height (beta1 = 0.17; P = .002) and body surface area (beta1 = 3.1; P = .039).

Additionally, data showed an association between NASH and reduced lateral E0 and septal E0 velocities and reduced mitral inflow velocity as measured by E-wave (r = 0.25; 95% CI, –0.49 to –0.02) and E-wave/A-wave ratio (r = –0.31; 95% CI, –0.51 to –0.09). Following multivariable analysis, NASH remained associated with reduced lateral velocity (beta1 = –0.91 cm/s; P = .015) and septal E0 velocity (beta1 = –0.89 cm/s; P = .07), E-wave (beta1 = –0.19 cm/s; P = .002), E-wave/A-wave ratio (beta1 = –4.15; P = .021), and deceleration time (beta1 = –14.52; P = .02).

“Whether diastolic dysfunction similarly portends a risk of future [heart failure] among patients with NAFLD and/or NASH remains unknown, and we eagerly await well-designed, prospective studies to characterize this relationship,” the researchers concluded. “Our study provides evidence that the pathogenesis of subclinical heart failure may relate to progressive NASH. Future studies with well-phenotyped populations and defined cardiovascular outcomes are needed to more fully define the risk of heart failure in patients with NAFLD.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.

A retrospective study revealed a link between nonalcoholic steatohepatitis and changes in myocardial structure as well as increased left atrial volume and left ventricular mass.

“We found that NASH was strongly associated with markers of diastolic dysfunction and also with ventricular wall thickening, indicative of early hypertrophy,” Tracey G. Simon, MD, from the Massachusetts General Hospital and Harvard Medical School, Boston, and colleagues wrote. “Such findings carry important clinical implications, as diastolic dysfunction is a well-described predictor of future [heart failure] risk within the general population.”

Between Jan. 1, 2005, and Aug. 1, 2016, 78 patients underwent elective bariatric surgery and transthoracic echocardiography within 12 months of surgery. Sixty-five of these patients met inclusion criteria. Median age was 47 years (range, 35-56.5) and etiologies included normal hepatic histology (n = 18), steatosis without ballooning or lobular inflammation (n = 33) and NASH defined by the presence of steatosis with ballooning or lobular inflammation (n = 14).

Compared with other patients in the study, those with NASH had higher median BMI (45 kg/m2 vs. 43.7 kg/m2; P = .003), were more likely to have diabetes (45% vs. 29%; P = .003), more likely to have a family history of type 1 coronary disease (67% vs. 19%; P = .016), and had higher median left atrial volume (28.6 mL/m2 vs. 24.8 mL/m2; P < .0001) and left ventricular mass (82.6 g/m2 vs. 78.6 g/m2; P < .0001).

After adjusting for age, sex, diabetes, hypertension, and BMI, the researchers found that NASH remained associated with increased left ventricular mass for height (beta1 = 7.16; P = 0.001) and left atrial volume for height (beta1 = 0.17; P = .002) and body surface area (beta1 = 3.1; P = .039).

Additionally, data showed an association between NASH and reduced lateral E0 and septal E0 velocities and reduced mitral inflow velocity as measured by E-wave (r = 0.25; 95% CI, –0.49 to –0.02) and E-wave/A-wave ratio (r = –0.31; 95% CI, –0.51 to –0.09). Following multivariable analysis, NASH remained associated with reduced lateral velocity (beta1 = –0.91 cm/s; P = .015) and septal E0 velocity (beta1 = –0.89 cm/s; P = .07), E-wave (beta1 = –0.19 cm/s; P = .002), E-wave/A-wave ratio (beta1 = –4.15; P = .021), and deceleration time (beta1 = –14.52; P = .02).

“Whether diastolic dysfunction similarly portends a risk of future [heart failure] among patients with NAFLD and/or NASH remains unknown, and we eagerly await well-designed, prospective studies to characterize this relationship,” the researchers concluded. “Our study provides evidence that the pathogenesis of subclinical heart failure may relate to progressive NASH. Future studies with well-phenotyped populations and defined cardiovascular outcomes are needed to more fully define the risk of heart failure in patients with NAFLD.” – by Talitha Bennett

Disclosure: The researchers report no relevant financial disclosures.