Prognostic Implications of Elevated Pulmonary Artery Pressure After ST-Segment Elevation Myocardial Infarction.
Elevated systolic pulmonary artery pressure (SPAP) after ST-segment elevation myocardial infarction (STEMI) has been associated with adverse outcome. However, little is known about the development of increased SPAP after STEMI treated with primary percutaneous coronary intervention. The aims of this study were to investigate the incidence and determinants of elevated SPAP (SPAP ≥36 mm Hg at 12 months) after first STEMI and to analyze its prognostic implications. A total of 705 patients (60 ± 12 years; 75% men; left ventricular ejection fraction [LVEF] 47 ± 9%) with first STEMI treated with primary percutaneous coronary intervention were evaluated. Two-dimensional echocardiography was available at baseline and 12-month follow-up. Data on all-cause mortality were collected at long-term follow-up. Incident elevated SPAP was present in 5% (n = 38) of patients. Patients with incident elevated SPAP were older (66 ± 12 vs 60 ± 11 years, p = 0.001), had more systemic hypertension (58% vs 30%, p <0.001) and lower LVEF (43 ± 9% vs 48 ± 8%, p <0.001) than their counterparts. Left atrial volume was larger (23 ± 11 vs 18 ± 6 ml/m(2), p = 0.006), and moderate to severe mitral regurgitation was more prevalent in patients with incident elevated SPAP (16% vs 7%, p = 0.05). Independent correlates of incident elevated SPAP at 12-month follow-up were age (odds ratio [OR] 1.04, 95% CI 1.01 to 1.08, p = 0.01), hypertension (OR 2.52, 95% CI 1.23 to 5.14, p = 0.01), baseline LVEF (OR 0.94, 95% CI 0.90 to 0.98, p = 0.003), and baseline left atrial volume (OR 1.08, 95% CI 1.03 to 1.12, p = 0.001). Incident elevated SPAP was independently associated with all-cause mortality (hazard ratio 3.84, 95% CI 1.76 to 8.39, p = 0.001). In conclusion, although the incidence of elevated SPAP after STEMI is low, its presence is independently associated with increased risk of all-cause mortality at follow-up.
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Marlieke L A
ML
Haeck
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Georgette E
GE
Hoogslag
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Helèn
H
Boden
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Matthijs A
MA
Velders
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Spyridon
S
Katsanos
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Ibtihal
I
Al Amri
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Philippe
P
Debonnaire
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Martin J
MJ
Schalij
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Hubert W
HW
Vliegen
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Jeroen J
JJ
Bax
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.
Nina Ajmone
NA
Marsan
Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands. Electronic address: v.delgado@lumc.nl.
Victoria
V
Delgado
D000368:Aged; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000453:epidemiology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000453:epidemiology; D016017:Odds Ratio; D062645:Percutaneous Coronary Intervention; D011379:Prognosis; D016016:Proportional Hazards Models; D011651:Pulmonary Artery / Q000503:physiopathology*; D011669:Pulmonary Wedge Pressure; D000072657:ST Elevation Myocardial Infarction / Q000453:epidemiology / Q000503:physiopathology / Q000601:surgery*; D013318:Stroke Volume; D013599:Systole; D016896:Treatment Outcome