INTRODUCTION: Hiatal hernia (HH) can cause left atrial (LA) compression and impair LA filling. We evaluated the cardiac effects of preload reduction and abdominal strain induced by Valsalva maneuver (VM) in large HH patients. METHODS: LA and left ventricular (LV) dimensions were measured using 2D transthoracic echocardiography at rest and during VM in HH patients (n=55, 70±10 years) and controls (n=22, 67±6 years). Biplane LV volumes (n=39) and mitral inflow pulse-wave Doppler parameters (n=27) were also evaluated. In HH patients, resting LA compression was graded qualitatively (none-mild or moderate-severe). RESULTS: In both controls and HH patients, VM significantly decreased LA (controls, 19±2 vs 16±3 mm/m2 ; HH, 16±5 vs 9±5 mm/m2 ) and LV diameters (22±3 vs 19±3 mm/m2 ; 21±3 vs 17±3 mm/m2 ) and LV volume (38±8 vs 26±10 mL/m2 ; 31±8 vs 19±9 mL/m2 ) (P<.001 for all). VM decreased LA diameter significantly more in HH patients than controls (-42% vs -16%, P<.001). HH patients with none-mild resting LA compression exhibited significantly greater LA diameter reduction than controls (-38±23% vs -16±13% P=.0003) despite similar resting LA diameters. LV volumes were similarly decreased by VM in HH patients and controls irrespective of resting LA compression severity indicating relative preservation of LV filling. LA diameter correlated inversely with early diastolic filling velocity during VM in HH patients (R=-.43, P=.03) but not controls (R=.18, P=.43). CONCLUSION: VM can markedly exacerbate LA compression in HH patients; however, LV filling is relatively less affected possibly due to augmented early diastolic filling. Conditions associated with decreased preload and increased intra-abdominal pressure may exacerbate the cardiac effects of large HH.
INTRODUCTION:Hiatal hernia (HH) can cause left atrial (LA) compression and impair LA filling. We evaluated the cardiac effects of preload reduction and abdominal strain induced by Valsalva maneuver (VM) in large HHpatients. METHODS: LA and left ventricular (LV) dimensions were measured using 2D transthoracic echocardiography at rest and during VM in HHpatients (n=55, 70±10 years) and controls (n=22, 67±6 years). Biplane LV volumes (n=39) and mitral inflow pulse-wave Doppler parameters (n=27) were also evaluated. In HHpatients, resting LA compression was graded qualitatively (none-mild or moderate-severe). RESULTS: In both controls and HHpatients, VM significantly decreased LA (controls, 19±2 vs 16±3 mm/m2 ; HH, 16±5 vs 9±5 mm/m2 ) and LV diameters (22±3 vs 19±3 mm/m2 ; 21±3 vs 17±3 mm/m2 ) and LV volume (38±8 vs 26±10 mL/m2 ; 31±8 vs 19±9 mL/m2 ) (P<.001 for all). VM decreased LA diameter significantly more in HHpatients than controls (-42% vs -16%, P<.001). HHpatients with none-mild resting LA compression exhibited significantly greater LA diameter reduction than controls (-38±23% vs -16±13% P=.0003) despite similar resting LA diameters. LV volumes were similarly decreased by VM in HHpatients and controls irrespective of resting LA compression severity indicating relative preservation of LV filling. LA diameter correlated inversely with early diastolic filling velocity during VM in HHpatients (R=-.43, P=.03) but not controls (R=.18, P=.43). CONCLUSION: VM can markedly exacerbate LA compression in HHpatients; however, LV filling is relatively less affected possibly due to augmented early diastolic filling. Conditions associated with decreased preload and increased intra-abdominal pressure may exacerbate the cardiac effects of large HH.