Elevated myocardial wall stress after percutaneous coronary intervention in acute ST elevation myocardial infraction is associated with increased mortality.


Journal

Echocardiography (Mount Kisco, N.Y.)
ISSN: 1540-8175
Titre abrégé: Echocardiography
Pays: United States
ID NLM: 8511187

Informations de publication

Date de publication:
08 2021
Historique:
revised: 12 05 2021
received: 22 02 2021
accepted: 11 06 2021
pubmed: 30 6 2021
medline: 14 9 2021
entrez: 29 6 2021
Statut: ppublish

Résumé

Despite early attempts to salvage myocardium-at-risk with percutaneous coronary intervention (PCI), changes in myocardial wall stress (MWS) leads to ventricular dilatation and dysfunction after acute ST-elevation myocardial infraction (STEMI). Whether this is transient or leads to long-term adverse outcomes major adverse cardiovascular events (MACE) is not known. We studied the association between MWS and MACE in patients after a successful PCI for acute STEMI. To study the MWS in percutaneously revascularized STEMI patients in relation to all-cause mortality and MACE. We prospectively enrolled 142 patients who presented to our tertiary care hospital with acute STEMI requiring emergent PCI. In addition to the standard clinical biomarkers, both end-systolic and end-diastolic MWS was calculated using our recently validated Echocardiographic indices. Patients were then prospectively followed up to an average of 16.5 (± 12.0) months to assess all-cause mortality and MACE. During the follow-up period, 9% of the patients died and 17% developed MACE. Patients who died had significantly elevated end-systolic WS compared to those who survived (mean ESWS, 80.01 ± 36.86 vs 59.28 ± 27.68). There was no significant difference in end-diastolic WS, left ventricular systolic function and peak troponin levels among survivors versus non-survivors. Elevated ESWS (>62.5 Kpa) and age remained the significant predictors of mortality on multivariate logistic analysis (OR 7.75, CI 1.33-73.86, P = .03; OR 1.16, CI 1.06-1.31, P = .002). Elevated ESWS measured by echocardiogram is associated with increased odds of long-term mortality in STEMI patients who have undergone emergent PCI. This finding can help clinicians to risk stratify high-risk patients.

Sections du résumé

BACKGROUND
Despite early attempts to salvage myocardium-at-risk with percutaneous coronary intervention (PCI), changes in myocardial wall stress (MWS) leads to ventricular dilatation and dysfunction after acute ST-elevation myocardial infraction (STEMI). Whether this is transient or leads to long-term adverse outcomes major adverse cardiovascular events (MACE) is not known. We studied the association between MWS and MACE in patients after a successful PCI for acute STEMI.
OBJECTIVES
To study the MWS in percutaneously revascularized STEMI patients in relation to all-cause mortality and MACE.
METHODS
We prospectively enrolled 142 patients who presented to our tertiary care hospital with acute STEMI requiring emergent PCI. In addition to the standard clinical biomarkers, both end-systolic and end-diastolic MWS was calculated using our recently validated Echocardiographic indices. Patients were then prospectively followed up to an average of 16.5 (± 12.0) months to assess all-cause mortality and MACE.
RESULTS
During the follow-up period, 9% of the patients died and 17% developed MACE. Patients who died had significantly elevated end-systolic WS compared to those who survived (mean ESWS, 80.01 ± 36.86 vs 59.28 ± 27.68). There was no significant difference in end-diastolic WS, left ventricular systolic function and peak troponin levels among survivors versus non-survivors. Elevated ESWS (>62.5 Kpa) and age remained the significant predictors of mortality on multivariate logistic analysis (OR 7.75, CI 1.33-73.86, P = .03; OR 1.16, CI 1.06-1.31, P = .002).
CONCLUSION
Elevated ESWS measured by echocardiogram is associated with increased odds of long-term mortality in STEMI patients who have undergone emergent PCI. This finding can help clinicians to risk stratify high-risk patients.

Identifiants

pubmed: 34184304
doi: 10.1111/echo.15131
pmc: PMC8410654
mid: NIHMS1714189
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1263-1271

Subventions

Organisme : NCATS NIH HHS
ID : UL1 TR001412
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NHLBI NIH HHS
ID : K08 HL131987
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR001413
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL152090
Pays : United States

Informations de copyright

© 2021 Wiley Periodicals LLC.

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Auteurs

Sharma Kattel (S)

Department of Medicine, Division of Cardiology, Jacob's School of Medicine and Biomedical Sciences, Buffalo, New York, USA.
Department of Medicine, Division of Cardiology, Yale School of Medicine, New Haven, Connecticut, USA.

Hardik Bhatt (H)

Department of Medicine, Division of Cardiology, Jacob's School of Medicine and Biomedical Sciences, Buffalo, New York, USA.

Sharda Gurung (S)

Department of Medicine, Division of Cardiology, Jacob's School of Medicine and Biomedical Sciences, Buffalo, New York, USA.

Badri Karthikeyan (B)

Department of Medicine, Division of Cardiology, Jacob's School of Medicine and Biomedical Sciences, Buffalo, New York, USA.

Umesh C Sharma (UC)

Department of Medicine, Division of Cardiology, Jacob's School of Medicine and Biomedical Sciences, Buffalo, New York, USA.

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