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Andersen, Mads Jønsson

0000-0002-9320-8227

Mayo Clinic

Department of Cardiology, Aarhus University Hospital, Denmark (M.J.A.).

Citations 12

The Hemodynamic Basis of Exercise Intolerance in Tricuspid Regurgitation

Circulation: Heart Failure | September 5, 2014 | Volume: 7 | Issue: 6 | Pages: 911-917

10.1161/circheartfailure.114.001575 | PMID 25190672

Background— Patients with severe tricuspid regurgitation (TR) frequently present with exertional fatigue and dyspnea, but the hemodynamic basis for exercise limitation in people with TR remains unclear. Methods and Results— Twelve subjects with normal left ventricular (LV) ejection fraction and grade ≥3 TR underwent high-fidelity invasive hemodynamic exercise testing with simultaneous expired gas analysis and were compared with 13 age- and sex-matched controls. At rest, TR subjects had lower pulmonary blood flow (3.6±0.4 versus 5.1±1.9 L/min; P =0.01), increased right atrial pressure (12±5 versus 4±1 mm Hg; P =0.0002), and higher pulmonary capillary wedge pressure (17±5 versus 9±3 mm Hg; P =0.0001). However, LV transmural pressure (pulmonary capillary wedge pressure−right atrial pressure), which reflects LV preload independent of right heart congestion and pericardial restraint, was similar in TR and controls (6±3 versus 4±2 mm Hg; P =0.3). With exercise, TR subjects displayed lower peak V O 2 (10.3±2.8 versus 13.8±4.2 mL/min per kg; P =0.02), lower pulmonary blood flow (6.4±1.3 versus 10.3±3.3 L/min; P =0.001), and less increase in pulmonary blood flow relative to V O 2 (+4.6±1.1vs +6.2±0.7; P =0.001). TR subjects displayed higher pulmonary capillary wedge pressure with exercise, but this was solely because of RA hypertension (27±9 versus 8±3 mm Hg; P <0.0001), because LV transmural pressure dropped with exercise in subjects with TR (−5±6 versus +3±3 mm Hg; P =0.0007), suggesting inadequate LV diastolic filling, despite high pulmonary capillary wedge pressure. Conclusions— Impaired exercise capacity in people with severe TR is related to low cardiac output reserve relative to metabolic needs, coupled with elevated systemic and pulmonary venous pressures. Left heart pressures are elevated with exercise in subjects with TR, despite low LV preload, secondary to enhanced ventricular interaction.
Exercise Hemodynamics in Patients With and Without Diastolic Dysfunction and Preserved Ejection Fraction After Myocardial Infarction

Circulation: Heart Failure | June 17, 2012 | Volume: 5 | Issue: 4 | Pages: 444-451

10.1161/circheartfailure.112.967919 | PMID 22705767

Background— Left ventricular diastolic dysfunction (DD) is common after myocardial infarction (MI) despite preservation of left ventricular ejection fraction, yet it remains unclear how or whether DD affects cardiac hemodynamics with stress. Methods and Results— Invasive hemodynamic exercise testing was performed in 46 patients with a recent MI and left ventricular ejection fraction >45% and in 10 healthy volunteers. MI patients were enrolled prospectively and divided into those with DD (MI+DD; left atrial volume index >34 mL/m 2 and diastolic E/e′ ratio>8; n=35) and those without DD (MI–DD; left atrial volume index <34 mL/m 2 and E/e′ ratio<8; n=11). All underwent a supine cycle ergometer test with simultaneous right heart catheterization and echocardiography. At rest, 10 patients in MI+DD (29%) had pulmonary capillary wedge pressure >15 (14±4 mm Hg), whereas none of the MI−DD (10±2 mm Hg) or controls (9±2 mm Hg) displayed pulmonary capillary wedge pressure elevation ( P =0.03). During exercise, an abnormal rise in pulmonary capillary wedge pressure (>25 mm Hg) was observed in 94% of MI+DD (36±6 mm Hg) compared with 36% of MI−DD (24±6 mm Hg) and none of the controls (16±6 mm Hg; P <0.0001). Exercise right atrial pressure was the highest in MI+DD followed by MI−DD and control (15±5 versus 9±4 versus 7±5 mm Hg; P <0.001), whereas no difference in cardiac index was found between groups. Conclusions— In post-MI patients with preserved ejection fraction and left ventricular DD, cardiac output with exercise is maintained at the expense of substantially increased filling pressure. DD and loss of diastolic reserve may promote progression from stage B to stage C heart failure after MI. (Circ Heart Fail. 2012;5:-451.)