Guo-Wei He

Background: Functional tricuspid regurgitation (TR) occurs in patients with rheumatic mitral valve disease even after mitral valve surgery. The aim of this study was to analyze surgical results of TR after previous successful mitral valve surgery. Methods: From September 1996 to September 2008, 45 patients with TR after previous mitral valve replacement underwent second operation for TR. In those, 43 patients (95.6%) had right heart failure symptoms (edema of lower extremities, ascites, hepatic congestion, etc.) and 40 patients (88.9%) had atrial fibrillation. Twenty-six patients (57.8%) were in New York Heart Association (NYHA) functional class III, and 19 (42.2%) in class IV. Previous operations included: 41 for mechanical mitral valve replacement (91.1%), 4 for bioprosthetic mitral valve replacement (8.9%), and 7 for tricuspid annuloplasty (15.6%). Results: The tricuspid valves were repaired with Kay's (7 cases, 15.6%) or De Vega technique (4 cases, 8.9%). Tricuspid valve replacement was performed in 34 cases (75.6%). One patient (2.2%) died. Postoperative low cardiac output (LCO) occurred in 5 patients and treated successfully. Postoperative echocardiography showed obvious reduction of right atrium and ventricle. The anterioposterior diameter of the right ventricle decreased to 25.5 ± 7.1 mm from 33.7 ± 6.2 mm preoperatively (P < 0. 05). Conclusion: TR after mitral valve replacement in rheumatic heart disease is a serious clinical problem. If it occurs or progresses late after mitral valve surgery, tricuspid valve annuloplasty or replacement may be performed with satisfactory results. Due to the serious consequence of untreated TR, aggressive treatment of existing TR during mitral valve surgery is recommended.

To compare the differences in nitric oxide (NO) release and endothelium-derived hyperpolarizing factor (EDHF)-mediated hyperpolarization between human radial artery (RA) and saphenous vein (SV) through direct measurement of NO and membrane potential. RA (n = 8), SV (n = 23), and surgical prepared SV (PV, n = 9, dilatation with normal saline solution at a pressure of 100 - 600 mmHg, 1 mmHg = 0.133 kPa) segments (5 mm long) taken from patients undergoing coronary artery bypass grafting were placed in an organ chamber. The NO-sensitive electrode and intracellular glass microelectrode was used to directly measure the NO release and the membrane potential changes in response to acetylcholine (ACh) and bradykinin (BK) before and after incubation with NG-nitro-L-arginine, indomethacin, and oxyhemoglobin. The basal release of NO in RA [(11.9 ± 1.8) nmol/L] was significantly greater than that in SV [(9.9 ± 2.8) nmol/L, P = 0.041]. BK-induced NO release in RA was lower than that in SV [for BK 10(-7) mol/L: (25.8 ± 3.6) nmol/L vs. (43.7 ± 8.2) nmol/L, P = 0.006]. Both basal and ACh- or BK-induced NO release in PV were significantly reduced [basal release: PV (3.4 ± 1.4) nmol/L; P = 0.006 vs. RA; P = 0.002 vs. SV; stimulated release: for ACh 10(-5) mol/L: PV (4.8 ± 3.2) nmol/L; vs. RA (28.6 ± 7.9) nmol/L, P = 0.005; vs. SV (27.4 ± 3.7) nmol/L, P = 0.003; for BK 10(-7) mol/L: PV (7.0 ± 3.6) nmol/L; vs. RA (25.8 ± 3.6) nmol/L, P = 0.016; vs. SV (43.7 ± 8.2) nmol/L, P = 0.004]. EDHF-mediated hyperpolarization was greater in RA than that in SV [ACh 10(-5) mol/L: (-9.7 ± 1.9) mV vs. (-4.5 ± 1.1) mV, n = 17, P = 0.002]. RA is superior to SV in terms of NO basal release and EDHF-mediated endothelial function. Surgical preparation and pressure dilatation may severely impair the NO-mediated endothelial function of SV, which may contribute to the poor long-term patency of SV coronary graft.

Background: We have investigated and compared nitric oxide (NO) release and endothelium‐derived hyperpolarizing factor (EDHF)‐mediated hyperpolarization in the human internal mammary artery (IMA), radial artery (RA), saphenous vein (SV), and coronary artery. Materials and Methods: Vessel segments taken from coronary artery bypass grafting or heart transplantation patients were placed in an organ chamber. NO‐sensitive electrode or intracellular glass microelectrode was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK). Results: The resting membrane potential of the smooth muscle cells of IMA, RA, and SV was‐58 ± 0.84 (n # 61),‐61 ± 1.3mV (n # 46, p # 0.03), and‐62 ± 0.9 mV (n # 23, p = 0.0001) respectively. BK‐(10–⁷M) induced EDHF‐mediated hyperpolarization (‐10.9 ± 1.5 mV, n # 7) in the IMA was significantly greater than that in RA (‐5.8 ± 0.9 mV, n # 6, p # 0.04) and SV (‐5.1 ± 0.5 mV, n = 8, p < 0.01). The basal release of NO in IMA (16.8 ± 1.9 nM) was significantly higher than that in RA (11.1 ± 1.0 nM, n # 12, p # 0.02) and in SV (9.9 ± 2.8 nM, n # 13, p < 0.001). The stimulated release of NO to BK in IMA was significantly greater than that in RA (44.3 ± 4.0 vs 25.8 ± 3.6 nM, n # 8, p # 0.004). The duration of NO release was longer in IMA than in RA or in SV. Conclusions: The basal and stimulated release of NO and EDHF‐mediated hyperpolarization in the IMA are significantly greater than that in the RA and SV. EDHF exists in all these human vessels. This study reveals the differences among human vessels regarding the endothelial function that have implications in vasospasm, coronary protection, or long‐term graft patency.

Objectives: Hyperkalemia in cardioplegia impairs the endothelium‐derived hyperpolarizing factor (EDHF)‐mediated function. This study examined the effect of procaine in cardioplegia on the EDHF‐mediated response in porcine coronary arteries. Methods: An isometric force study was performed in a myograph. Two rings taken from the same artery (diameter 200–450 μm) were incubated with Krebs solution (group I) or 20 mM K⁺ (group II) with/without procaine (1 mM) at 37°C for 1 hour. The EDHF‐mediated relaxation was induced by bradykinin (BK,‐10 ˜‐6.5 log M) after U₄₆₆₁₉ (‐8 log M, in group I) or K⁺‐precontraction (in group II) in the presence of indomethacin (7 μM), N^G‐nitro‐L‐arginine (300 μM), and hemoglobin (20 μM). The membrane potential of a single smooth muscle cell was measured by a microelectrode after superfusion with Krebs solution with/without procaine for 1 hour. Results: The EDHF‐mediated relaxation was increased by the treatment with procaine with the EC₅₀ shifted leftward (97.3 ± 0.6% vs. 83.0 ± 5.1% at‐7 log M and 99.4 ± 0.6% vs. 96.7 ± 1.6% at‐6.5 log M, p < 0.05; EC₅₀.‐8.57 ± 0.24 vs.‐7.92 ± 0.23 log M, p < 0.05). Procaine decreased the BK‐induced hyperpolarization from‐72.3 ± 0.7 mV to‐68.8 ± 0.8 mV (‐6.5 log M, p < 0.01). The EDHF‐mediated relaxation in arteries exposed to 20 mM K⁺ was not altered by procaine (49.9 ± 7.4% vs. 55.8 ± 7.6%, p > 0.05). Conclusions: In the coronary arteries, procaine has a depolarizing effect but it enhances EDHF‐mediated relaxation. Addition of procaine in cardioplegia did not change the EDHF‐mediated endothelial function.

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Background We aimed to confirm the mid-term results of the new method combined with bone marrow-derived mesenchymal stem cells (MSCs) transplantation and transmyocardial drilling revascularization (TMDR) with degradable stent incorporated with basic fibroblast growth factor and heparin. Methods The miniswine underwent acute myocardial infarction by ligation of the left anterior descending coronary artery. Transmyocardial channels with 3.5 mm diameter (TMDR) were made by mechanical drilling in the infarction territory and basic fibroblast growth factor stents were implanted into the channels. Animals were randomly divided into the following four groups (n=6 in each): control; II: MSCs implantation; III: TMDR+stent implantation; IV: TMDR+stent implantation+MSCs implantation. Three months postoperatively, ECG-gated single photon emission computed tomography, histopathological examination, and reverse transcription-polymerase chain reaction were carried out. Results Left ventricular ejection fraction and myocardial perfusion were significantly improved in group IV than that in other groups (PPP<0.05). Conclusion Three months after operation, MSCs transplantation combined with TMDR and degradable stent significantly improved cardiac function, enhanced neovascular density, reduced infarcted size, improved ventricular remodeling, and reduced cardiac myocyte apoptosis, and therefore provides strong information for clinical trial.

We developed a new method—transmyocardial drilling revascularization (TMDR) with absorbable stent incorporated with basic fibroblast growth factor (bFGF) and heparin. The present study tested the effect of this method with transplantation of bone marrow-derived stem cells (BMSCs) in acute myocardial infarction. Infarction was produced in mini-swine by ligating the left anterior descending (LAD) coronary artery. TMDR of 3.0 mm in diameter was made by mechanical drilling in the infarcted area. The animals that had LAD ligation were divided into six groups according to the procedures followed (n = 6 in each): control; T (TMDR); C (cell implantation); TS (TMDR+stent implantation); TC (TMDR+cell implantation); TSC (TMDR+stent implantation+cell implantation). Left ventricular (LV) function, myocardial perfusion, vascular density, and histological and morphological analyses were evaluated pre-operatively and at 30 min and 6 weeks post-operatively. Six weeks after operation, the above indices were significantly better in the TSC group than in other groups (P < 0.001 compared with the control group, and P < 0.05 or 0.01 compared with the TS and TC groups), although TS and TC also showed better results than the control group (P < 0.05). We have demonstrated in a pig model that an intramyocardial stent implanted with slow release of bFGF, heparin, and BMSC transplantation may significantly increase LV function, cardiac blood flow, and vascular density. Therefore, the present study may provide a new method for the surgical treatment of myocardial infarction.