Héctor Banchs

The Metabolic Syndrome in Hispanics - The Role of Inflammation

We report clinical and molecular mechanisms relating the pro-inflammatory and anti-inflammatory process in the development of the components of the metabolic syndrome, emphasizing the cardiovascular problems developed in these groups of patients, especially the Hispanic population. Namely, the incidence, component characteristics and complications of the metabolic syndrome in island Puerto Ricans are described and evidence is presented supporting the fact that the metabolic syndrome may be milder in Puerto Rico than in the mainland United States because it is characterized by less aggressive coronary artery disease and a relatively normal lipid profile. Moreover, data supports the fact that increased serum cholesterol levels produce less myocardial infarctions in Puerto Rico than in mainland Hispanics and Caucasians.

HDL as a Biomarker of Rejection in Heart Transplant

Background: One hundred once patients underwent heart transplants due to multiple causes. These patients included 36 females and 65 males whose mean age was 51 years.

The Metabolic Syndrome in Hispanics – The Role of Insulin Resistance and Inflammation

The acknowledgment of the metabolic syndrome (MetS) as a pathological entity is one of the most important advancements in the management of cardiovascular disease in the last 2 decades. Increasing awareness and research of this syndrome has led to a deeper understanding of how different metabolic risk factors such as inflammation, insulin resistance and vascular pathologies such as coronary heart disease (CHD) interact and aggravate one another. The existence of MetS may imply uniformity in pathology across a range of populations. However, this is not the case: the mechanisms that underlie MetS and the cardiometabolic consequences they hold may very well vary between ethnicities. The following chapter aims to encompass MetS from its most fundamental principles with a focus on inflammation and insulin resistance to the novel research pertaining to its pathophysiology and management, with an emphatic eye on the Hispanic population.

170 OUTCOMES OF HEART TRANSPLANT RECIPIENTS USING BASILIXIMAB, A CHIMERIC ANTI-INTERLEUKIN-2 RECEPTOR MONOCLONAL ANTIBODY: THE PUERTO RICAN EXPERIENCE.

Background Immunosuppressive therapy in heart transplantation is evolving. Induction immunotherapy in addition to standard triple therapy at the time of cardiac transplantation with cytolytic antibodies has been used in recipients with pretransplant renal impairment and to prevent rejection. Recently anti-interleukin-2 receptor monoclonal antibodies have being used for these purposes. A retrospective study of 58 heart transplant recipients was conducted to assess the effect of basiliximab, a chimeric anti-interleukin-2 receptor monoclonal antibody on biopsy proved acute rejection, creatinine clearance, serum creatinine, hospitalizations due to infection, and mortality 1 year after transplantation. Methods A total of 58 patients charts were reviewed. The dose of basiliximab 20 mg infusion on day 0 and day 4 was selected. All patients received triple immunosuppressive therapy with cyclosporine or tacrolimus, mycophenolate mofetil, and prednisone at 24 hours post-transplant. Among the patients in the induction group 23 were males and 4 females with a mean age of 43.68 (16-62) years. In the group of patients without induction therapy, 20 were males and 11 females with a mean age of 49.58 (11-60) years. Both groups had similar pretransplant characteristics with a mean creatinine clearance of 73.97 (SD 30.54) mL/min and an average serum creatinine of 1.152 mg/dL (SD 0.24) in the induction group and 84 mL/min (SD25.49) and 1.023 mg/dL (SD.36) in the the group without induction respectively. Analysis of 0-3-, 4-6-, 7-12-month intervals post-transplant was performed. The incidence of acute rejection episodes, patient survival, and hospitalizations due to infection was analyzed. Results Twenty-seven patients received induction therapy with basiliximab and 31 patients did not. At 0-3 month-, 4-6-month intervals and overall period, basiliximab reduced significantly the proportion of patients who experienced confirmed biopsy acute rejection episodes (p = .005) but not at the 7-12-month interval. There were no statistical differences in hospitalizations due to infection among groups (p = .2).There were two deaths in the basiliximab group, one due to infection and the other due to acute graft failure at 0-3 months post-transplant. There was no difference in post-transplant renal function between both groups at any interval studied. Conclusion Induction therapy with basiliximab significantly reduced the number of acute rejection within the first year after transplantation, without a negative impact on patients renal function, risk of infection, or mortality.

3 HISPANICS WITH THE METABOLIC SYNDROME SHOWED HIGHER INCIDENCE OF ATRIAL FIBRILLATION.

Atrial fibrillation (AF) is the most frequent arrhythmia after the sixth decade. The incidence in (P) with metabolic syndrome (MS) and diabetes mellitus type II (DM) is not known. A retrospective analysis was undertaken in 173 p. with MS-DM with insignificant coronary disease. The mean age was 60 years. 57% were males and 42.5 females. The mean blood sugar on admission was 169 mg/dL. The mean body mass was 30 kg/m2. The ejection fraction was subnormal (52 ± 8%) when compared to our normal group (62 ± 12%), p < .0001. The end-systolic dimension of the left atrium was higher in the MS-DM (46 ± 10 mm) when compared to the normal group (40 ± 8 mm), p < .05. The incidence of (AF) in the MS was 12.9% when compared to the control group (5.9%), p < .001. Causes of this higher incidence are (1) ischemia to the sinus node due to atherosclerosis or vasoconstriction of the sinus node (SN) artery due to an elevated concentration of angiotensin II peripherally, intracoronary, and in the atrial tissue; (2) remodeling of the SN due to left ventricular dysfunction; (3) remodeling of the left and right atrium; (4) hyperinsulinemia influencing the SN through NA+-K+ ATPase; (5) aging; (6) abnormalities of QT dispersion. All of these mechanisms will be discussed.