Pathophysiologic Vasodilation in Cardiogenic Shock and Its Impact on Mortality.

arterial pressure hospital mortality microcirculation shock, cardiogenic vasoconstriction

Journal

Circulation. Heart failure
ISSN: 1941-3297
Titre abrégé: Circ Heart Fail
Pays: United States
ID NLM: 101479941

Informations de publication

Date de publication:
25 Jul 2024
Historique:
medline: 26 7 2024
pubmed: 26 7 2024
entrez: 25 7 2024
Statut: aheadofprint

Résumé

Cardiogenic shock (CS) mortality remains near 40%. In addition to inadequate cardiac output, patients with severe CS may exhibit vasodilation. We aimed to examine the prevalence and consequences of vasodilation in CS. We analyzed all patients hospitalized at a CS referral center who were diagnosed with CS stages B to E and did not have concurrent sepsis or recent cardiac surgery. Vasodilation was defined by lower systemic vascular resistance (SVR), higher norepinephrine equivalent dose, or a blunted SVR response to pressors. Threshold SVR values were determined by their relation to 14-day mortality in spline models. The primary outcome was death within 14 days of CS onset in multivariable-adjusted Cox models. This study included 713 patients with a mean age of 60 years and 27% females; 14-day mortality was 28%, and 38% were vasodilated. The median SVR was 1308 dynes•s•cm Pathophysiologic vasodilation is prevalent in CS and independently associated with an increased risk of death. CS vasodilation can be identified by SVR <800 dynes•s•cm

Sections du résumé

BACKGROUND UNASSIGNED
Cardiogenic shock (CS) mortality remains near 40%. In addition to inadequate cardiac output, patients with severe CS may exhibit vasodilation. We aimed to examine the prevalence and consequences of vasodilation in CS.
METHODS UNASSIGNED
We analyzed all patients hospitalized at a CS referral center who were diagnosed with CS stages B to E and did not have concurrent sepsis or recent cardiac surgery. Vasodilation was defined by lower systemic vascular resistance (SVR), higher norepinephrine equivalent dose, or a blunted SVR response to pressors. Threshold SVR values were determined by their relation to 14-day mortality in spline models. The primary outcome was death within 14 days of CS onset in multivariable-adjusted Cox models.
RESULTS UNASSIGNED
This study included 713 patients with a mean age of 60 years and 27% females; 14-day mortality was 28%, and 38% were vasodilated. The median SVR was 1308 dynes•s•cm
CONCLUSIONS UNASSIGNED
Pathophysiologic vasodilation is prevalent in CS and independently associated with an increased risk of death. CS vasodilation can be identified by SVR <800 dynes•s•cm

Identifiants

pubmed: 39051115
doi: 10.1161/CIRCHEARTFAILURE.124.011827
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

e011827

Auteurs

Miguel A Chavez (MA)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

McHale Anderson (M)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Christos P Kyriakopoulos (CP)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Monte Scott (M)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Elizabeth Dranow (E)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Eleni Maneta (E)

Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City (E.M., R.H., S.G.D.).

Rana Hamouche (R)

Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City (E.M., R.H., S.G.D.).

Iosif Taleb (I)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).
Division of Cardiology, Department of Medicine, University of California, San Diego, La Jolla (I.T.).

Jacy Leon (J)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Benjamin Kogelschatz (B)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Jake Goldstein (J)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Filio Billia (F)

Peter Munk Cardiac Centre, University of Toronto, ON, Canada (F.B.).

David A Baran (DA)

Department of Cardiovascular Medicine, Cleveland Clinic Heart, Vascular, and Thoracic Institute, Weston, FL (D.A.B.).

Behnam Tehrani (B)

Inova Fairfax Hospital, Falls Church, VA (B.T.).

Matt Goodwin (M)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Craig H Selzman (CH)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Joseph E Tonna (JE)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

James C Fang (JC)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Stavros G Drakos (SG)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City (E.M., R.H., S.G.D.).

Thomas C Hanff (TC)

Division of Cardiovascular Medicine, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City (M.A.C., M.A., C.P.K., M.S., E.D., I.T., J.L., B.K., J.G., M.G., C.H.S., J.E.T., J.C.F., S.G.D., T.C.H.).

Classifications MeSH