'Edge-to-edge' mitral valve repair: the ace of hearts.
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Biomedical subjects
Publications and source records attributed to Mario Chiavarelli.
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PURPOSE: The main aim of the present study was to investigate skeletal muscle oxidative metabolism in heart transplant recipients (HTR) by noninvasive tools. METHODS: Twenty male HTR (age 50.4 +/- 2.6 yr; mean +/- SE) and 17 healthy untrained age-matched controls (CTRL) performed an incremental exercise (IE) and a series of constant-load (CLE) moderate-intensity exercise tests on a cycloergometer. The following variables were determined: heart rate (HR); breath-by-breath pulmonary O2 uptake (VO2); and skeletal muscle (vastus lateralis) oxygenation indices by continuous-wave near-infrared spectroscopy. Changes in concentration of deoxygenated hemoglobin (Hb) and myoglobin (Mb) (Delta[deoxy(Hb + Mb)]), expressed as a fraction of values obtained during a transient limb ischemia, were taken as an index of skeletal muscle O2 extraction. "Peak" values were determined at exhaustion during IE. Kinetics of adjustment of variables were determined during CLE. RESULTS: VO2peak, HRpeak, and Delta[deoxy(Hb + Mb)] peak were significantly lower in HTR than in CTRL (17.1 +/- 0.7 vs 34.0 +/- 1.9 mL.kg(-1).min(-1), 133.8 +/- 3.8 vs 173.0 +/- 4.8 bpm, and 0.42 +/- 0.03 vs 0.58 +/- 0.04, respectively). In HTR, Delta[deoxy(Hb + Mb)] increase at submaximal workloads was steeper than in CTRL, suggesting an impaired O2 delivery to skeletal muscles, whereas the lower Delta[deoxy(Hb + Mb)] peak values suggest an impaired capacity of O2 extraction at peak exercise. VO2 and HR kinetics during CLE were significantly slower in HTR than in CTRL, whereas, unexpectedly, no significant differences were found for Delta[deoxy(Hb+Mb)] kinetics (mean response time: 21.3 +/- 1.1 vs 20.2 +/- 1.2 s). CONCLUSION: The findings confirm the presence of both "central" (cardiovascular) and "peripheral" (at the skeletal muscle level) impairments to oxidative metabolism in HTR. The noninvasiveness of the measurements will allow for serial evaluation of the patients, in the presence and/or absence of rehabilitation programs.
Cardiac myxomas are primary cardiac tumors. In some cases of atrial myxoma, the standard left atriotomy alone does not enable safe tumor resection and easy access to the mitral valve. We report the cases of 2 patients with huge left atrial myxomas associated with severe mitral valve regurgitation who underwent an inverted T-shaped biatrial incision for tumor excision and mitral repair. This approach reduces tumor fragmentation and permits good mitral valve exposure.
Angiotensin (Ang) II is now recognized to be a mediator of a wide variety of inflammatory processes. This study investigated renin-angiotensin system (RAS) components and a number of inflammatory mediators in left ventricular biopsies from 2-vessel disease unstable angina (UA) (n=43) and stable angina (SA) (n=15) patients undergoing coronary bypass surgery. Biopsy samples from 6 patients undergoing valve replacement for mitral stenosis served as controls. UA patients were randomly assigned to angiotensin-converting enzyme (ACE)-inhibitor (ramipril), AT1 antagonist (valsartan), or placebo and treated during the 5 days preceding coronary bypass surgery, performed from 6 to 9 days after coronary angiography. During coronary angiography coronary blood flow was measured and samples were obtained from aorta and coronary sinus for determination of Ang I and Ang II gradients. The hearts of UA patients produced Ang II in a greater amount than in SA patients (P<0.01). UA biopsy samples showed numerous DR+ cells, identified as lymphocytes, macrophages, and endothelial cells. Reverse-transcriptase polymerase chain reaction showed overexpression of AGTN, ACE, and AT1-R genes, as well as upregulation of TNF-alpha, IL-6, IFN-gamma, and iNOS genes (P<0.01), with no differences between nonischemic and potentially ischemic areas. AGTN, ACE, and cytokine genes were mainly localized on endothelial cells. Ramipril and valsartan markedly decreased the expression levels of TNF-alpha, IL-6, and iNOS, and, to a lesser extent, of IFN-gamma genes, but did not affect the number of DR+ cells, with no significant difference between the 2 treatments. These results show that locally generated Ang II amplifies the immunomediated inflammatory process of coronary microvessels occurring in unstable angina.
A case of asymptomatic aortic valve fibroelastoma was diagnosed by transthoracic and transesophageal echocardiography in a 77-year-old man. A 2nd tumor was found at surgery. Both fibroelastomas were removed surgically without aortic valve replacement. During surgical excision of a cardiac fibroelastoma, the entire area surrounding the lesion should be inspected carefully for additional lesions. Such lesions can be missed on echocardiographic evaluation.
This study investigated whether the myocardium is involved in the acute inflammatory reaction associated with bursts of unstable angina (UA). We looked for the presence of activated DR+ inflammatory cells and the expression patterns, localization, and immunostaining identification of genes for cytokines (IL-1beta, TNF-alpha, IL-6, and IFN-gamma), MCP-1, and iNOS in the left ventricle biopsies from 2-vessel disease anginal patients, 24 with UA and 12 with stable angina (SA), who underwent coronary bypass surgery. Biopsy specimens from 6 patients with mitral stenosis who underwent valve replacement were examined as control hearts (CHs). Plasma levels of IL-2 soluble receptor (sIL-2R) were measured as a marker of systemic immune reaction. In CHs, DR+ cells were undetectable, and cytokine and iNOS mRNA expression were negligible. UA patients had higher sIL-2R levels than SA patients (P<0.01), and their biopsy specimens showed both numerous DR+ cells identified as lymphocytes, macrophages, endothelial cells, and elevated expression levels of cytokine and iNOS genes (from 2.4- to 6.1-fold vs SA; P<0.01). Cytokine and iNOS genes and proteins were localized in endothelial cells without involvement of myocytes. IL-1beta and MCP-1 mRNAs were nearly undetectable. No significant differences were found in the number of DR+ cells, levels of cytokine, and iNOS genes between potentially ischemic and nonischemic left ventricle areas. In SA specimens, DR+ cells were very rare and only mRNAs for TNF-alpha and iNOS genes were overexpressed versus CHs. These results indicated that an acute immunomediated inflammatory reaction, essentially involving coronary microvessels, is demonstrable in UA patients.
AIMS: The purpose of this study was to determine that the administration of an angiotensin converting enzyme (ACE) inhibitor enalapril would confer protection against doxorubicin-induced experimental heart failure, and attenuate the development of left ventricular dysfunction. METHODS: Seventeen dogs were chronically instrumented with an intracoronary catheter and received doxorubicin weekly for 4 weeks. Animals were assigned to two groups: group 1: untreated heart failure; and group 2: simultaneous enalapril administration (5 mg twice a week). Hemodynamic data were obtained at week 0 and 12. Echocardiography was performed weekly. RESULTS: Survival improved with simultaneous enalapril administration (36% in group 1 vs. 100% in group 2, P=0.04). The increase in the left ventricular end-diastolic pressure was significantly reduced at week 12 (17+/-1 mmHg in group 1 vs. 9+/-1 mmHg in group 2, P=0.0042). The fall in left ventricular stroke work index was significantly prevented (52% in group 1 vs. 21% in group 2, P=0.006). The increase in right ventricular end-diastolic diameter was significantly reduced by enalapril prophylaxis. CONCLUSION: Simultaneous treatment with enalapril was beneficial in the prevention of doxorubicin-induced cardiomyopathy.
BACKGROUND: There has been an increase in the number of elderly patients considered for cardiac surgery. Several reports have documented acceptable morbidity and mortality in patients 80 years and older. The results from surgical patients 85 years and older were analyzed. METHODS: The records of 89 consecutive patients 85 years and older having cardiac operations between June 1993 and May 1999 were retrospectively reviewed. For purposes of statistical analysis follow-up was considered as a minimum of one office visit to the surgeon, cardiologist, or internist at least 1 month postoperatively. RESULTS: Eighty-seven patients underwent coronary artery grafting and two patients had mitral valve replacement. Follow-up was 100% complete. The operative mortality rate was 12.3%; probability of in-hospital death was 8.2%; risk-adjusted mortality rate was 3.2%. The complication rate was 31.5%. The actuarial 1-, 3-, and 5-year survivals were as follows: 75%, 67%, and 40%. Multivariate predictors of 30-day mortality were preoperative EF, less than 30% (p = 0.029) and postoperative renal failure (p = 0.0039). CONCLUSIONS: Cardiac surgery can be performed in patients 85 years and older with good results. There is an associated prolonged hospital stay for elderly patients. Consistent successful outcomes can be expected in this patient population with selective criteria identifying risk factors.