Yu-Qin Yan1, Lin Liu2, Shuo Sun2, Ying-Qing Feng2, Jie Li2, Yu-Qing Huang2. 1. Department of Cardiology, People's Hospital of Shenzhen Baoan District, Shenzhen, China. 2. Department of Cardiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Abstract
Background: Although the evidence was still limited, some studies suggested that childhood malnutrition might affect cardiac function and structure in adulthood. To address the knowledge gap, this study investigated if the Great Chinese Famine exposure during early life had affected left ventricular hypertrophy (LVH). Methods: This research was a cross-sectional study. It included participants who had cardiac ultrasound assessments and were born in Guangdong, China, from 1 October 1952 to 30 September 1964. They were classified according to their exposure period to famine, namely, no exposure, fetal-, early-, mid-, and late childhood. Multivariate logistic regression and subgroup analysis have been conducted to determine the odds ratio (OR) and confidence intervals (CIs) between famine exposure and LVH. Results: This research included 2,543 participants, 1,612 women, their mean age was 59.07 ± 3.65 years, and 704 participants had LVH. LVH prevalence was 122 (23.6%), 87 (25.1%), 133 (27.3%), 184 (29.2%), and 178 (31.7%), in non-, fetal-, early-, mid-, and late-childhood exposed groups, respectively (p = 0.031), while in the non-exposed group, the ORs for developing carotid plaque as a result of fetal, early-, mid- to late-childhood exposure were 1.08 (95% CI: 0.76, 1.59, p = 0.619), 1.24 (95% CI: 1.03, 1.79, p = 0.031), 1.49 (95% CI: 1.10, 2.01, p = 0.009), and 1.64 (95% CI: 1.25, 2.18, p = 0.001), respectively (p for trend = 0.003). There was no interactive effect between gender, obesity, or hypertension history with how the famine influenced LVH, as the subgroups analyses demonstrated (all p for interaction > 0.05). Conclusion: This research has demonstrated the potential relationship between Great Chinese Famine exposure during childhood and LVH in adults.
Background: Although the evidence was still limited, some studies suggested that childhood malnutrition might affect cardiac function and structure in adulthood. To address the knowledge gap, this study investigated if the Great Chinese Famine exposure during early life had affected left ventricular hypertrophy (LVH). Methods: This research was a cross-sectional study. It included participants who had cardiac ultrasound assessments and were born in Guangdong, China, from 1 October 1952 to 30 September 1964. They were classified according to their exposure period to famine, namely, no exposure, fetal-, early-, mid-, and late childhood. Multivariate logistic regression and subgroup analysis have been conducted to determine the odds ratio (OR) and confidence intervals (CIs) between famine exposure and LVH. Results: This research included 2,543 participants, 1,612 women, their mean age was 59.07 ± 3.65 years, and 704 participants had LVH. LVH prevalence was 122 (23.6%), 87 (25.1%), 133 (27.3%), 184 (29.2%), and 178 (31.7%), in non-, fetal-, early-, mid-, and late-childhood exposed groups, respectively (p = 0.031), while in the non-exposed group, the ORs for developing carotid plaque as a result of fetal, early-, mid- to late-childhood exposure were 1.08 (95% CI: 0.76, 1.59, p = 0.619), 1.24 (95% CI: 1.03, 1.79, p = 0.031), 1.49 (95% CI: 1.10, 2.01, p = 0.009), and 1.64 (95% CI: 1.25, 2.18, p = 0.001), respectively (p for trend = 0.003). There was no interactive effect between gender, obesity, or hypertension history with how the famine influenced LVH, as the subgroups analyses demonstrated (all p for interaction > 0.05). Conclusion: This research has demonstrated the potential relationship between Great Chinese Famine exposure during childhood and LVH in adults.
Authors: Giuseppe Mancia; Robert Fagard; Krzysztof Narkiewicz; Josep Redon; Alberto Zanchetti; Michael Böhm; Thierry Christiaens; Renata Cifkova; Guy De Backer; Anna Dominiczak; Maurizio Galderisi; Diederick E Grobbee; Tiny Jaarsma; Paulus Kirchhof; Sverre E Kjeldsen; Stéphane Laurent; Athanasios J Manolis; Peter M Nilsson; Luis Miguel Ruilope; Roland E Schmieder; Per Anton Sirnes; Peter Sleight; Margus Viigimaa; Bernard Waeber; Faiez Zannad; Josep Redon; Anna Dominiczak; Krzysztof Narkiewicz; Peter M Nilsson; Michel Burnier; Margus Viigimaa; Ettore Ambrosioni; Mark Caufield; Antonio Coca; Michael Hecht Olsen; Roland E Schmieder; Costas Tsioufis; Philippe van de Borne; Jose Luis Zamorano; Stephan Achenbach; Helmut Baumgartner; Jeroen J Bax; Héctor Bueno; Veronica Dean; Christi Deaton; Cetin Erol; Robert Fagard; Roberto Ferrari; David Hasdai; Arno W Hoes; Paulus Kirchhof; Juhani Knuuti; Philippe Kolh; Patrizio Lancellotti; Ales Linhart; Petros Nihoyannopoulos; Massimo F Piepoli; Piotr Ponikowski; Per Anton Sirnes; Juan Luis Tamargo; Michal Tendera; Adam Torbicki; William Wijns; Stephan Windecker; Denis L Clement; Antonio Coca; Thierry C Gillebert; Michal Tendera; Enrico Agabiti Rosei; Ettore Ambrosioni; Stefan D Anker; Johann Bauersachs; Jana Brguljan Hitij; Mark Caulfield; Marc De Buyzere; Sabina De Geest; Geneviève Anne Derumeaux; Serap Erdine; Csaba Farsang; Christian Funck-Brentano; Vjekoslav Gerc; Giuseppe Germano; Stephan Gielen; Herman Haller; Arno W Hoes; Jens Jordan; Thomas Kahan; Michel Komajda; Dragan Lovic; Heiko Mahrholdt; Michael Hecht Olsen; Jan Ostergren; Gianfranco Parati; Joep Perk; Jorge Polonia; Bogdan A Popescu; Zeljko Reiner; Lars Rydén; Yuriy Sirenko; Alice Stanton; Harry Struijker-Boudier; Costas Tsioufis; Philippe van de Borne; Charalambos Vlachopoulos; Massimo Volpe; David A Wood Journal: Eur Heart J Date: 2013-06-14 Impact factor: 29.983