Predictors of late outcomes after concomitant tricuspid valve repair with left-sided valve surgery.

BACKGROUND: Concomitant tricuspid valve (TV) repair is a safe and effective procedure to protect against late moderate or greater tricuspid regurgitation (TR) after left-sided valve surgery, but studies regarding its late outcomes and recurrent TR are limited. This study aimed to reveal the late outcomes and explore the predictors of mortality and recurrent TR among patients who underwent concomitant TV repair with left-sided valve surgery. METHODS AND RESULTS: This study included 645 patients (mean age, 69.7 years; 44% male) who underwent concomitant TV repair with left-sided valve surgery (mitral valve surgery in 594 cases, aortic valve surgery in 172 cases) from 2006-2020. Preoperative TR was grade 4, 3, and less than 2 in 85, 235, and 325 patients, respectively. The median follow-up period was 4.6 (IQR 1.7-7.8) years. The in-hospital or 30-day mortality was 1.7% (n = 11). Regarding long-term outcomes after TV repair, 90.3% and 80.8% achieved 5- and 10-year survival, respectively, while 96.1% and 88.8% achieved 5- and 10-year freedom from recurrent TR, respectively. The following were independent predictors of overall mortality on multivariate analysis in patients with preoperative TR grade ≥ 3: prior pacemaker implantation, preoperative renal dysfunction, diabetes mellitus and NYHA class ≥ 3. Also, suture annuloplasty and ring type of ring annuloplasty were not independent risk factors for recurrent TR, classified as grade ≥ 3. CONCLUSIONS: Concomitant TV repair with left-sided valve surgery had acceptable outcomes in terms of survival and TR durability. In patients with preoperative TR grade ≥ 3, preoperative patient status had negative impacts on prognosis.

Short- and Midterm outcomes of modified robotic tricuspid annuloplasty for secondary tricuspid regurgitation.

BACKGROUND: Despite the growing popularity of robotically assisted mitral repair, robotically assisted tricuspid repair has not been widely adopted. We assessed the safety and feasibility of robotic tricuspid annuloplasty with continuous sutures for tricuspid regurgitation (TR). METHODS AND RESULTS: We studied consecutive 68 patients (median age, 74 years) with secondary TR who underwent tricuspid annuloplasty using continuous sutures with (n = 61) and without mitral valve repair (n = 7) from 2018 to 2021. Robotic tricuspid annuloplasty consists of continuous sutures with flexible prosthetic band to the tricuspid annulus using two V-Loc barbed sutures (Medtronic Inc., Minneapolis, MN). Concomitant maze procedure was performed in 45 (66%) patients. Robotic tricuspid annuloplasty with continuous sutures was successfully performed. There was no in-hospital or 30-day mortality; 65 patients (96%) did not experience major surgery-related complications. Preoperatively, the TR grade was mild in 20 (29%) patients and mildly higher in 48 (71%). Postoperatively, the TR severity significantly improved, with TR grade mildly higher in 9% at hospital discharge and 7% at 1-year follow-up (p < 0.001). The 1-year and 2-year freedom rates from heart failure were 98% and 95%, respectively. CONCLUSIONS: Robotic tricuspid annuloplasty with continuous sutures is safe and feasible alone or concomitant with mitral valve repair. It offered sustained improvement in TR severity and might prevent heart failure readmission.

Thoracic endovascular aortic repair with collateral vessels from the femoral artery to Adamkiewicz's artery.

Identification of the Adamkiewicz's artery (AKA) prior to the operation is one of the spinal cord ischaemia preventive measures. A 75-year-old man presented with the rapid expansion of thoracic aortic aneurysm. Collateral vessels from the right common femoral artery to the AKA were observed on preoperative computed tomography angiography. The stent graft was successfully deployed through the contralateral side via a pararectal laparotomy to avoid collateral vessel injury supplying the AKA. This case highlights the significance of preoperative identification of collateral vessels to the AKA.

Type A aortic dissection with left coronary malperfusion.

Left coronary artery malperfusion is a fatal complication of acute type A aortic dissection. However, effective treatment strategies have not yet been established. Herein, we report two cases of left coronary artery malperfusion successfully treated with different preoperative catheter interventions, followed by a central aortic repair. Preoperative coronary intervention ensuring the blood flow to the left coronary artery might be essential if a coronary angiogram was performed prior to the diagnosis and treatment.

Cardiovascular reactions for whole-body thermal therapy with a hot pack and Waon therapy.

Background: Waon therapy (WT) is the predominant thermal therapy for chronic heart failure in Japan, involving use of a far-infrared dry sauna. As sauna therapy requires certain equipment not readily available in hospitals, we tested the use of whole-body hot pack thermal therapy (HPTT). We compared the magnitude of skin vasodilation post-HPTT with that post-WT.Methods: We recruited 19 healthy men (age [mean ± S.D.]: 26.8 ± 4.6 years) and employed a simple randomized crossover design. The HPTT required subjects to remain in a supine position on a bed for at least 10 min. Hot packs were then applied on the back, lower abdomen, and popliteal regions for 15 min (warming phase). Participants continued bed rest for 30 min (heat-retention phase) after removal of the hot pack. WT was performed as previously described. Blood pressure (BP), heart rate (HR), tympanic temperature (TT), and peak and average flow velocity of the right radial artery (PFV and AFV, respectively) and right brachial artery (BA) diameter were measured during HPTT and WT.Results: HR, TT, PFV, and AFV persistently and significantly increased during warming and heat-retention phases of HPTT. In WT, HR and TT significantly increased during warming but decreased and plateaued during heat-retention. BP did not change significantly after either therapy; however, BA was dilated equally in both (HPTT: 3.70 ± 0.57 ⇒ 4.05 ± 0.59 mm, p = .001; WT: 3.63 ± 0.63 ⇒ 3.93 ± 0.61 mm, p < .001).Conclusion: HPTT may be equivalent to WT with respect to vasodilation response of the skin.

Stent implantation and optical frequency domain imaging with carbon dioxide for chronic total occlusion in the superficial femoral artery.

A 68-year-old female was presented with claudication in the left lower leg. She underwent angiography with carbon dioxide (CO2) because she had a history of anaphylactic shock to iodinated contrast medium. It revealed total occlusion of the left superficial femoral artery (SFA), and subsequently endovascular therapy (EVT) was performed by an antegrade approach from the left common femoral artery. After stent implantation, we performed optical frequency domain imaging (OFDI) using CO2 as contrast medium. OFDI has been extensively studied in the coronary circulation; however, its use in the peripheral arterial circulation is scarce. We present a case of stent implantation and OFDI using CO2 as an ancillary tool during EVT for SFA lesions in the patient with contraindication to iodinated contrast medium.

Endothelial dysfunction, macrophage infiltration and NADPH oxidase-dependent superoxide production were attenuated by erythropoietin in streptozotocin-induced diabetic rat aorta.

Erythropoietin (EPO) has been used for the management of renal anemia. Recent studies suggest the pleiotropic properties of EPO in various tissues such as brain, kidney and vasculature. Diabetes mellitus is a major risk for development of vascular impairment. The aim of the present study was to investigate the hypothesis that EPO would be beneficial in inhibiting diabetic macroangiopathy. Recombinant human EPO (rHuEPO; 150 U/kg, 3 times/week, s.c.) was administered to streptozotocin-induced diabetic rats for 4 weeks. Streptozotocin (65 mg/kg, i.v.) significantly increased macrophage infiltration and adhesion molecules, monocyte chemoattractant protein-1 and osteopontin mRNA levels in the aorta. These inflammatory changes were suppressed by rHuEPO. Vasodilation in response to acetylcholine in the aortic ring was impaired in the diabetic rats, and improved by rHuEPO. rHuEPO inhibited the aortic expression of mRNA for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the NADPH oxidase-dependent superoxide production and the increase in plasma malondialdehyde concentration in diabetic rats. rHuEPO also decreased the level of the receptor for advanced glycation end products in the aorta. We also found an increased expression of phospho-Akt and endothelial nitric oxide synthase and plasma NOx level in the rHuEPO-treated group. On the other hand, rHuEPO did not affect blood glucose levels, hemoglobin A(1c), blood pressure or hematocrit in diabetic rats. These results indicate that rHuEPO exerts pleiotropic antioxidant and anti-inflammatory properties in diabetic rat aorta.

Anti-atherogenic effects of the combination therapy with olmesartan and azelnidipine in diabetic apolipoprotein E-deficient mice.

Many studies have aimed to identify anti-atherogenic agents in cardiovascular medicine. We have recently demonstrated that the combination therapy with olmesartan (OLM), an angiotensin II receptor blocker, and azelnidipine (AZL), a dihydroprydine calcium-channel blocker, improves endothelial function in diabetic Apolipoprotein-deficient (ApoE(-/-)) mice. In the present study, we examined whether this combination therapy also inhibits atherosclerosis in mice. We used male control and streptozocin-induced diabetic ApoE(-/-) mice. Diabetic ApoE(-/-) mice were orally treated for 5 weeks with vehicle (Untreated), OLM (30 mg/kg/day), AZL (10 mg/kg/day), their combination (OLM+AZL), or hydralazine (HYD, 5 mg/kg/day) as an antihypertensive control. At 5 weeks, systolic blood pressure was significantly elevated in Untreated but was normalized in OLM+AZL and HYD. The atherosclerosis area in the thoracic aorta, perivascular fibrosis and medial thickness of the coronary arteries were increased in Untreated and were ameliorated in OLM+AZL but not in HYD. Staining with a fluorescent probe dihydroethidium showed that production of reactive oxygen species was increased in Untreated, and ameliorated in OLM+AZL. Consistent with these findings, macrophage infiltration in the kidney and the expression of receptor for advanced glycation end-products in the heart, kidney and liver were increased in Untreated and were all ameliorated in OLM+AZL, associated with up-regulation of endothelial NO syntheses (eNOS). In conclusion, the combination therapy with OLM and AZL exerts anti-atherogenic effect in diabetic ApoE(-/-) mice through suppression of oxidative stress and activation of eNOS, independent of its blood pressure-lowering effects. Clinically, this combination therapy may be useful for patients with hypertension, hyperlipidemia and diabetes.

Erythropoietin attenuated vascular dysfunction and inflammation by inhibiting NADPH oxidase-derived superoxide production in nitric oxide synthase-inhibited hypertensive rat aorta.

Erythropoietin (EPO), used clinically for renal anemia, reportedly exerts beneficial pleiotropic effects in various tissues. Recent studies suggest that nitric oxide (NO) plays an important role in EPO-induced tissue protection. The present study investigated whether recombinant human EPO (rHuEPO) exhibits vasoprotective effects even in the NO synthase-inhibited state. Rats that received a NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), in drinking water (0.7 mg/ml) were treated with rHuEPO (75 U/kg, s.c.) three times a week for 2 weeks. The administration of rHuEPO to L-NAME-treated rats had no effect on hematocrit values or increased blood pressure. Vasodilation in response to acetylcholine in the aortic ring was impaired in the L-NAME-treated rats, and improved by rHuEPO. Immunohistochemical staining revealed that infiltration by macrophages and expression of osteopontin were enhanced in the L-NAME-treated rat aorta, and the overexpression was suppressed by rHuEPO. rHuEPO also attenuated medial hyperplasia. Activation of Akt signaling was evident in rHuEPO-treated rats as the increased expression of phosphorylated Akt. rHuEPO enhanced the expression of antioxidant enzymes such as Cu/Zn-superoxide dismutase and heme oxygenase-1 in the aorta. In addition, rHuEPO reduced NADPH oxidase-dependent superoxide production and enhanced the expression of suppressor of cytokine signaling-1(SOCS-1) in the L-NAME-treated rat aorta. These results suggest that a low dose of rHuEPO results in the normalization of endothelial function and vascular inflammation beyond hematopoiesis even in a pharmacologically NO synthase-inhibited state. These effects might be due to the antioxidant properties of rHuEPO. SOCS-1 overexpression would play an important role in suppressing NADPH oxidase activation.

Essential role of bone marrow for microvascular endothelial and metabolic functions in mice.

RATIONALE: We have previously demonstrated that the importance of endothelium-derived hyperpolarizing factor (EDHF) increases as the vessel size decreases and that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF in animals and humans, for which endothelial nitric oxide synthase (eNOS) is the major source. Recent studies have suggested the important role of the bone marrow (BM) in modulating cardiovascular and metabolic functions. OBJECTIVE: We aimed to examine whether BM plays a role in modulating microvascular endothelial and metabolic functions in mice, and if so, to elucidate the mechanisms involved. METHODS AND RESULTS: Male eNOS(-/-) mice were transplanted with BM cells from wild-type (WT) or eNOS(-/-) mice and were maintained for 6 weeks. Endothelium-dependent relaxations and hyperpolarizations of mesenteric arteries to acetylcholine were reduced in eNOS(-/-) mice and were markedly improved when transplanted with WT-BM but not with eNOS(-/-)-BM. The enhanced component of endothelium-dependent relaxations was abolished by catalase, indicating that the improved responses were mediated by H(2)O(2). In contrast, no such beneficial effect was noted in the aorta. Reduced plasma adiponectin levels and impaired glucose tolerance in eNOS(-/-) mice were also improved by WT-BM transplantation. Neuronal nitric oxide synthase (nNOS) in mesenteric arteries of eNOS(-/-) mice was significantly upregulated only when transplanted with WT-BM. Importantly, the beneficial effects of WT-BM transplantation were absent in eNOS(-/-)/adiponectin(-/-) or eNOS(-/-)/nNOS(-/-) mice. CONCLUSIONS: These results provide the first evidence that BM plays an important role in modulating microvascular endothelial and metabolic functions, for which adiponectin and nNOS may be involved.

Antibody against interleukin-6 receptor attenuates left ventricular remodelling after myocardial infarction in mice.

AIMS: The plasma level of interleukin-6 (IL-6) has been reported to be associated with left ventricular (LV) remodelling after myocardial infarction (MI). The present study was designed to examine whether anti-IL-6 receptor antibody (MR16-1) prevents the development of LV remodelling after MI. METHODS AND RESULTS: Balb/c male mice were subjected to MI by ligating the left anterior descending coronary artery. The mice were then treated with an intraperitoneal injection of MR16-1 (500 microg/body) or control IgG. MR16-1 decreased the myocardial myeloperoxidase activity and monocyte chemoattractant protein-1 concentration in the infarct region, concomitant with decreases in neutrophil and macrophage infiltration 3 days after ligation, while infarct size was comparable between the control IgG- and MR16-1-treated mice. At 7 days after ligation, MR16-1 significantly suppressed matrix metalloproteinase-2 activity in the infarct region. Furthermore, the MR16-1-treated mice demonstrated a reduction in LV dilatation and an improvement in LV contractile function compared with the control IgG-treated mice at 7 and 28 days after surgery, leading to an improvement in survival rate (80.6 vs. 59.5%, P < 0.05) at 28 days after surgery. The beneficial effects of MR16-1 were accompanied by histological suppression of cardiomyocyte hypertrophy and interstitial fibrosis in the non-infarct region. CONCLUSION: Administration of MR16-1 after MI suppressed myocardial inflammation, resulting in the amelioration of LV remodelling. Neutralization of the IL-6 receptor is a potentially useful strategy for protecting hearts from LV remodelling after MI.