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3.
Am J Cardiovasc Dis ; 12(4): 205-211, 2022.
Article in English | MEDLINE | ID: mdl-36147786

ABSTRACT

Unloading the heart may aid recovery after acute cardiac volume-overload (AVO). We experimentally investigated whether unloading the heart after AVO by heterotopic transplantation histologically impacts myocardial outcome. Thirty-two syngeneic Fisher 344 rats underwent surgery for abdominal arterial-venous fistula to induce AVO. Seven hearts were heterotopically transplanted one day after AVO to simulate a non-working state of the left ventricle (AVO+Tx). In addition, six rats without AVO or surgery (Normal) and five rats with sham surgery (Sham) served as controls. Myocardial outcome was studied using histology and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analysis for hypoxia inducible factor 1alpha (HIF1α), inducible nitric oxide synthase (iNOS), E-selectin, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), vascular endothelial growth factor alpha (VEGFα), matrix metalloprotease 9 (MMP9), chitinase-3-like protein (YKL-40) and transforming growth factor beta (TGFß). Relative ischemia of the right ventricle and septal intramyocardial arteries was decreased in AVO+Tx as compared with AVO (0.04±0.01 vs. 0.09±0.02, PSU, P=0.040 and 0.04±0.01 vs. 0.16±0.02, PSU, P=0.008, respectively). Quantitative RT-PCR showed an increase in the expression of iNOS, YKL-40 and VEGFα, and decrease in ANP in AVO+Tx as compared with AVO (5.78±1.23 vs. 2.46±0.81, P=0.039, 22.39±5.22 vs. 10.79±1.70, P=0.039 and 1.15±0.22 vs. 0.60±0.08, P=0.030, and 1.32±0.16 vs. 2.85±0.70, P=0.039, respectively). Unloading the heart by heterotopic transplantation induces early ischemic recovery of intramyocardial arteries after AVO. A non-working state reverses acute ischemic myocardial injury after AVO.

6.
J Thorac Cardiovasc Surg ; 164(1): 107-114.e1, 2022 07.
Article in English | MEDLINE | ID: mdl-33069428

ABSTRACT

OBJECTIVE: To explore the currently unknown association between history of cancer at the time of coronary artery bypass grafting (CABG) and long-term survival. METHODS: All patients (n = 82,137) undergoing isolated first-time CABG in Sweden during 1997-2015 were included in this retrospective population-based cohort study. Individual patient data from the SWEDEHEART registry and 4 other mandatory nationwide health care registries were merged. Multivariable Cox proportional hazards regression and competing risk models adjusted for age and gender were used to assess associations between history of cancer, and long-term all-cause, cardiovascular and cancer mortality. Median follow-up was 9.0 years (interquartile range, 4.8-13.1). RESULTS: Altogether, 6819 (8.3%) of the patients had a history of cancer. The annual prevalence increased from 3.8% in 1997 to 14.8% in 2015. Patients with a history of cancer were older (72 vs 66 years; P < .001) and had more comorbidities. Long-term all-cause mortality was significantly greater in patients with a history of cancer (45.7% vs 22.9% at 10 years; adjusted hazard ratio, 1.33; 95% confidence interval [CI], 1.28-1.38, P < .001). According to the competing risk models, history of cancer was associated with an increased risk for cancer death (subdistribution hazard ratio, 2.45; 95% CI, 2.28-2.63, P < .001) but not cardiovascular death (subdistribution hazard ratio, 0.88; 95% CI, 0.83-0.94, P < .001). CONCLUSIONS: The proportion of patients undergoing CABG with a history of cancer has increased over time. History of cancer at the time of surgery is associated with increased cancer deaths over time but not cardiovascular deaths. The same cardiovascular prognosis after CABG can be expected regardless of cancer history.


Subject(s)
Coronary Artery Disease , Neoplasms , Cohort Studies , Coronary Artery Bypass/adverse effects , Humans , Registries , Retrospective Studies , Risk Factors , Treatment Outcome
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13.
JTCVS Tech ; 6: 30-31, 2021 Apr.
Article in English | MEDLINE | ID: mdl-34318132
15.
JTCVS Open ; 8: 377-378, 2021 Dec.
Article in English | MEDLINE | ID: mdl-36004067
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