Commentary : Collective responsibility in combating injection drug use-related endocarditis

publishedVersionNon peer reviewe

Is mood associated with perception of recovery? Preoperative depression versus postoperative delirium after cardiac surgery

The author alone is responsible for the Invited Commentary, which does not necessarily reflect the policy of the Journal.publishedVersionNon peer reviewe

Commentary : A pile of vital cells is needed to treat myocardial infarction

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Autonomic nerves in myocardial sleeves around caval veins : Potential role in cardiovascular mortality?

Background: Quantitative changes in the cardiac autonomic nervous system may play an important role in the pathogenesis of various cardiovascular diseases. In the present morphological analysis, we aimed to study autonomic nerve density in myocardial sleeves and surrounding fibro-fatty tissue around caval veins. We correlated the nerve distribution with cardiovascular mortality and a history of atrial fibrillation. Materials and Methods: A total of 24 autopsied adult hearts were excised together with the superior and inferior vena cava and grouped according to the immediate and underlying causes of death (cardiovascular vs. non-cardiovascular), and documented heart rhythm history (atrial fibrillation vs. sinus rhythm). The density of autonomic nerves was quantified by measuring the area of immunohistochemical staining for sympathetic (tyrosine hydroxylase, TH) and parasympathetic (choline acetyltransferase, CHAT) nerves and ganglia. Growth-associated protein 43 (GAP43) was used as a neural growth marker. Results: The mean density of TH-positive nerves in the superior vena cava myocardial sleeves was significantly decreased between groups with documented underlying cardiovascular vs. non-cardiovascular cause of death (mean density ± standard deviation (SD): 704.81±1016.41 µm2/mm2 vs. 2391.01±1841.37 µm2/mm2; P =.008). Similarly, the nerve density of GAP43-positive nerves in the superior vena cava myocardial sleeves was significantly lower in subjects with documented underlying cardiovascular cause of death (mean density ± SD: 884.74±1240.16 µm2/mm2 vs. 2132.89±1845.89 µm2/mm2; P =.040). The mean age was significantly higher in subjects with documented underlying cardiovascular vs. non-cardiovascular cause of death (mean age ± SD: 69.2±11.9 years, vs. 57.5±11.2 years, P =.016). No differences were found in nerve densities of TH-positive (953.01±1042.93 µm2/mm2 vs. 919.26±1677.58 µm2/mm2), CHAT-positive (180.8±532.9 µm2/mm2 vs. 374.22±894.76 µm2/mm2), and GAP43-positive nerves (593.58±507.97 µm2/mm2 vs. 1337.34±1747.69 µm2/mm2) in myocardial sleeves around the inferior vena cava between groups with documented immediate cardiovascular vs. non-cardiovascular cause of death. Similarly, no differences were found between groups with documented underlying cardiovascular vs. non-cardiovascular cause of death (TH: 717.23±887.31 µm2/mm2 vs. 1365.51±2149.10 µm2/mm2; CHAT: 256.18±666.86 µm2/mm2 vs. 368.53±959.47 µm2/mm2; GAP43: 661.21±839.51 µm2/mm2 vs. 1759.90±2008.80 µm2/mm2). Moreover, there was no association found in nerve densities between subjects with documented atrial fibrillation vs. sinus rhythm (TH: 235.07±425.69 µm2/mm2 vs. 1166.08±1563.84 µm2/mm2; CHAT: 648.59±1017.33 µm2/mm2 vs. 175.31±641.65 µm2/mm2; GAP43: 990.17±1315.18 µm2/mm2 vs. 1039.86±1467.23 µm2/mm2). Conclusions: Decrease of superior vena cava myocardial sleeve sympathetic nerves may be associated with cardiovascular mortality and/or aging. No difference in autonomic innervation was found between subjects with documented atrial fibrillation vs. sinus rhythm.publishedVersionPeer reviewe

Ascending aortic wall degeneration in patients with bicuspid versus tricuspid aortic valve

Background: The magnitude of ascending aortic degeneration in patients with bicuspid aortic valves (BAV) is controversial. Methods: The aim of this study was to investigate ascending aortic wall degeneration in patients with BAV as compared with tricuspid aortic valves (TAV). The ascending aortic wall of 67 consecutive patients was processed for histology and immunohistochemistry. The extent of surgery and wall degeneration were investigated. Unadjusted survival was evaluated by Kaplan–Meier analysis. Median follow-up for patients with BAV and TAV was 3.8 years (interquartile range [IQR] 3.5–4.1) and 3.7 years (IQR 3.4–3.9), respectively. Results: There were 33 patients with BAV and 34 with TAV. Mid-ascending aorta diameter was 54 mm (IQR 50–60). Replacement of the aortic valve, together with an ascending aortic prosthesis, was more frequent in BAV vs TAV patients (24% vs. 3%, P = 0.013). However, medial fibrosis, elastic fiber thinning, incremental medial degeneration and smooth muscle cell nuclei loss were less prominent in BAV vs TAV patients (0.1 ± 0.4 vs. 0.8 ± 1.4, P = 0.016; 0.6 ± 1.4 vs. 1.6 ± 2.0, P = 0.027; 1.7 ± 0.7 vs. 2.2 ± 0.8, P = 0.045 and 2.3 ± 1.5 vs. 3.2 ± 1.3, P = 0.026, respectively). Conclusions: Since degeneration of the ascending aortic wall was seldom prominent, histopathology alone may not support the need for surgery of the dilated ascending aorta in BAV patients as compared with TAV patients.publishedVersionPeer reviewe

Human Pulmonary Vein Myocardial Sleeve Autonomic Neural Density and Cardiovascular Mortality

Myocardial sleeves around pulmonary veins (PVs) are highly innervated structures with heterogeneous morphological and electrophysiological characteristics. Autonomic nerve dysfunction in the myocardium may be associated with an increased risk of cardiovascular morbidity and mortality. This article studied autonomic neural remodeling in myocardial sleeves around PVs and atrial-PV ostia with immunohistochemical and morphometric methods with clinicopathological correlations. PVs were collected from 37 and atrial-PV ostia from 17 human autopsy hearts. Immunohistochemical analysis was performed using antibodies against tyrosine hydroxylase (TH), choline acetyltransferase (CHAT), and growth-associated protein 43 (GAP43). In the PV cohort, subjects with immediate cardiovascular cause of death had significantly decreased sympathetic nerve density in fibro-fatty tissue vs those with non-cardiovascular cause of death (1624.53 vs 2522.05 µm2/mm2, p=0.038). In the atrial-PV ostia cohort, parasympathetic nerve density in myocardial sleeves was significantly increased in subjects with underlying cardiovascular cause of death (19.48 µm2/mm2) than subjects with underlying non-cardiovascular cause of death with no parasympathetic nerves detected (p=0.034). Neural growth regionally varied in sympathetic nerves and was present in most of the parasympathetic nerves. Heterogeneous autonomic nerve distribution and growth around PVs and atrial-PV ostia might play a role in cardiovascular morbidity and mortality. No association in nerve density was found with atrial fibrillation.acceptedVersionPeer reviewe

Myocardial interaction of apixaban after experimental acute volume overload

Objective: Acute volume overload (AVO) induces early ischemia-like changes in intramyocardial arteries. We investigated whether the Factor Xa (FXa) inhibitor apixaban interacts with the myocardium early after AVO. Methods: Fifty-five syngeneic Fisher rats underwent surgical abdominal aortocaval fistula to induce AVO. Among them, 17 rats were treated with apixaban (10 mg/kg/day). The myocardial outcome was studied using histological analysis and by measuring atrial natriuretic peptide (ANP) and matrix metalloprotease 9 (MMP9) gene expression. Results: After 3 days, the total number of intramyocardial arteries was significantly increased in the AVO+apixaban (AVO+A) group compared with that in the AVO group (12.0 ± 1.2 and 10.2 ± 1.5, point score units, respectively). In the AVO+A group, there were significantly more edematous nuclei in myocardial arteries in the right and left ventricle compared with that in the AVO group. ANP and MMP9 expression levels continued to increase significantly in the AVO+A group compared with those in the AVO group. Conclusion: Apixaban interacts with intramyocardial arteries in the left and right ventricles after AVO and ANP and MMP9 expression levels increased. Thus, the myocardial effect of Factor Xa inhibition needs to be monitored after AVO.publishedVersionPeer reviewe

Early reversibility of histological changes after experimental acute cardiac volume-overload

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 (TGFβ). 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.publishedVersionPeer reviewe