Mitral regurgitation: anatomy is destiny.

Mitral regurgitation (MR) occurs when any of the valve and ventricular mitral apparatus components are disturbed. As MR progresses, left ventricular remodelling occurs, ultimately causing heart failure when the enlarging left ventricle (LV) loses its conical shape and becomes globular. Heart failure and lethal ventricular arrhythmias may develop if the left ventricular end-systolic volume index exceeds 55 ml/m2. These adverse changes persist despite satisfactory correction of the annular component of MR. Our goal was to describe this process and summarize evolving interventions that reduce the volume of the left ventricle and rebuild its elliptical shape. This 'valve/ventricle' approach addresses the spherical ventricular culprit and offsets the limits of treating MR by correcting only its annular component.

Multi-channel electrical bioimpedance: a non-invasive method to simultaneously measure cardiac output and individual arterial limb flow in patients with cardiovascular disease.

BACKGROUND: Cardiac output is the fundamental determinant of peripheral blood flow however; optimal regional tissue perfusion is ultimately dependant on the integrity of the arterial conduits that transport flow. A complete understanding of tissue perfusion requires knowledge of both cardiac and peripheral blood flow. Existing noninvasive devices do not simultaneously assess the cardiac and peripheral circulations. Multi-channel electrical bioimpedance (MEB) measures cardiac output and peripheral flow simultaneously. OBJECTIVES: Assessment of the accuracy of MEB to measure cardiac output in patients with clinical heart failure (group 1) and to measure regional arterial limb flow in patients with exertional leg pain clinically thought to have peripheral arterial disease (group 2). METHODS: Cardiac output was measured by MEB in 44 patients with moderate to severe clinical heart failure (group 1) and was compared to a cardiac output measured by 2D-Echo Doppler. Peripheral blood flow (regional ankle and arm flow) was measured by MEB in another group of 25 patients with exertional leg pain clinically thought to be claudication (group 2). The MEB ankle/arm flow ratio (AAI index) was then compared to a conventional ankle/brachial pressure ratio (ABI index). RESULTS: There was excellent correlation between the mean cardiac index by MEB (2.01 l/min/m(2)) and by 2D-Echo Doppler (2.06 l/min/m(2)) and bias and precision was 0.05 (2.4%) and +/-0.48 l/min/m(2) (+/-23%), respectively. The correlation was maintained for each measurement over a wide range of cardiac indices. There was good correlation between AAI and ABI measurements (P < 0.05). CONCLUSIONS: MEB accurately measures cardiac output in patients with moderate to severe clinical heart failure and accurately measures regional arterial limb flow in patients with peripheral arterial disease.

Multi-channel electrical bioimpedance: a new noninvasive method to simultaneously measure cardiac and peripheral blood flow.

OBJECTIVES: We sought to assess the ability of a new multi-channel electrical bioimpedance (MEB) methodology to accurately measure both cardiac blood flow and peripheral limb blood flow. BACKGROUND: Cardiac output is the primary determinant of peripheral blood flow; however, optimal regional tissue perfusion is ultimately dependent on the patency of the arterial conduits that transport that flow. A complete understanding of regional tissue perfusion requires knowledge of both cardiac and peripheral blood flow. Existing noninvasive devices do not simultaneously assess the cardiac and peripheral circulations. METHODS: Cardiac blood flow (cardiac output) was measured by MEB in 30 healthy volunteers and was compared to a 2D-Echo Doppler cardiac output. Peripheral blood flow (regional ankle and arm flow) was measured by MEB in 15 healthy volunteers. The MEB ankle/arm flow ratio (AAI index) was then compared to a conventional ankle/brachial pressure ratio (ABI index). RESULTS: There was good correlation between the mean cardiac index by MEB (3.08 l/min/m2) and by Echo Doppler (3.13 l/min/m2) and bias and precision was 0.051 (1.6%) and +/-0.52 l/min/m2 (+/-17%), respectively. The close correlation was maintained for each measurement over a wide range of cardiac indices. There was good correlation between AAI and ABI measurements (p < 0.05) with a sensitivity of 100% and specificity of 100%. CONCLUSIONS: MEB methodology can precisely measure cardiac output and peripheral limb flow in healthy volunteers.

Surgical ventricular restoration in the treatment of congestive heart failure due to post-infarction ventricular dilation.

OBJECTIVES: The purpose of this study was to test how surgical ventricular restoration (SVR) affects early and late survival in a registry of 1,198 post-anterior infarction congestive heart failure (CHF) patients treated by the international Reconstructive Endoventricular Surgery returning Torsion Original Radius Elliptical shape to the left ventricle (RESTORE)team. BACKGROUND: Congestive heart failure may be caused by late left ventricular (LV) dilation after anterior infarction. The infarcted segment is often akinetic rather than dyskinetic because early reperfusion prevents transmural necrosis. Previously, only dyskinetic areas were treated by operation. Surgical ventricular restoration reduces LV volume and creates a more elliptical chamber by excluding scar in either akinetic or dyskinetic segments. METHODS: The RESTORE group applied SVR to 1,198 post-infarction patients between 1998 and 2003. Early and late outcomes were examined, and risk factors were identified. RESULTS: Concomitant procedures included coronary artery bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality after SVR was 5.3% (8.7% with mitral repair vs. 4.0% without repair; p < 0.001). Perioperative mechanical support was uncommon (<9%). Global systolic function improved postoperatively. Ejection fraction (EF) increased from 29.6 +/- 11.0% preoperatively to 39.5 +/- 12.3% postoperatively (p < 0.001). The left ventricular end-systolic volume index (LVESVI) decreased from 80.4 +/- 51.4 ml/m(2) preoperatively to 56.6 +/- 34.3 ml/m(2) postoperatively (p < 0.001). Overall five-year survival was 68.6 +/- 2.8%. Logistic regression analysis identified EF or=80 ml/m(2), advanced New York Heart Association (NYHA) functional class, and age >or=75 years as risk factors for death. Five-year freedom from hospital readmission for CHF was 78%. Preoperatively, 67% of patients were NYHA functional class III or IV and postoperatively, 85% were class I or II. CONCLUSIONS: Surgical ventricular restoration improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent five-year outcome.

Heart failure following anterior myocardial infarction: an indication for ventricular restoration, a surgical method to reverse post-infarction remodeling.

Anterior myocardial infarction produces abrupt left ventricular (LV) dysynergy and global systolic dysfunction. Rapid intense neurohumoral activation, infarct expansion, and early ventricular chamber dilatation all contribute to restoring a normal stroke volume despite a persistently depressed ejection fraction. Continued neurohumoral activation provokes late remodeling of the remote non-infarcted myocardium, characterized by an abnormal progressively increasing LV volume/mass ratio that leads to further LV remodeling. Heart failure is a progressive disorder of LV remodeling. Heart failure from post-infarction remodeling is unique because of the persistent non-functioning scar that self- perpetuates abnormal loading conditions and neurohumoral activation. Medical therapy attenuates remodeling and improves survival but does not change the size of the scar. Surgical ventricular restoration to exclude the non-functioning infarct from the ventricular cavity decreases ventricular volumes, increases global ejection fraction, attenuates neurohumoral activation and yields an excellent 5-year survival. Combined medical and surgical therapy is recommended in this patient population.

Surgical ventricular restoration: the RESTORE Group experience.

Congestive heart failure may be caused by late left ventricular (LV) dilation following anterior infarction. Early reperfusion prevents transmural necrosis, and makes the infarcted segment akinetic rather than dyskinetic. Surgical ventricular restoration (SVR) reduces LV volume and creates a more elliptical chamber by excluding scar in either akinetic or dyskinetic segments. The international RESTORE group applied SVR in a registry of 1198 post-infarction patients between 1998 and 2003. Early and late outcomes were examined and risk factors identified.Concomitant procedures included coronary artery bypass grafting in 95%, mitral valve repair in 22%, and mitral valve replacement in 1%. Overall 30-day mortality after SVR was 5.3% (8.7% with mitral repair vs. 4.0% without repair, p < .001) Perioperative mechanical support was uncommon (< 9%). Global systolic function improved postoperatively, as ejection fraction increased from 29.6 +/- 11.0% to 39.5 +/- 12.3% (p < .001) and left ventricular end systolic volume index decreased from 80.4 +/- 51.4 ml/m(2) to 56.6 +/- 34.3 ml/m(2) (p < .001). Overall 5-year survival was 68.6 +/- 2.8%, Logistic regression analysis identified EF < or = 30%, LVESVI > o = 80 ml/m(2), advanced NYHA functional class, and age > or =75 years as risk factors for death. Five-year freedom from hospital readmission for CHF was 78%. Preoperatively, 67% of patients were class III or IV, and postoperatively 85% were class I or II.SVR improves ventricular function and is highly effective therapy in the treatment of ischemic cardiomyopathy with excellent 5-year outcome.

Glucose-insulin-potassium infusion for myocardial protection during off-pump coronary artery surgery.

BACKGROUND: The purpose of this randomized, double-blind, placebo-controlled pilot study was to determine the effectiveness of an intravenous glucose-insulin-potassium (GIK) infusion in preventing myocardial damage and maintaining cardiac performance in patients undergoing "off-pump" myocardial revascularization. METHODS: Forty-six adult patients undergoing elective off-pump coronary artery bypass received either normal saline or a GIK infusion immediately after the induction of anesthesia through the first 12 hours of intensive care unit convalescence. Measurements of blood glucose, circulating creatine kinase MB and troponin I concentrations, as well as cardiac index (CI) and mixed venous oxygen saturation (SvO2), were obtained immediately before starting the infusion (baseline) and at 6, 12, and 24 hours post-initial coronary artery occlusion. RESULTS: Five patients (8%) requiring cardiopulmonary bypass were excluded from data analysis. Twenty patients received saline. Twenty-one received GIK. Blood glucose was significantly higher in the GIK group. The concentration of circulating creatine kinase MB and troponin I significantly increased over time after off-pump coronary artery bypass, with no significant intergroup differences. Cardiac index and SvO2 did not differ significantly between groups. CONCLUSIONS: A GIK infusion protocol commonly used as an adjunct to reperfusion therapy for acute myocardial infarction causes insulin-resistant hyperglycemia in elective off-pump coronary artery bypass patients with no demonstrable benefit. The finding of significant release of cardio-specific enzymes in individual patients implies an ongoing need to develop more effective strategies for myocardial protection during off-pump coronary artery bypass.