OBJECTIVE

This study aims to determine the clinical profile and incidence of in-hospital outcomes of patients who underwent coronary artery bypass graft surgery (CABG) under the Philippine Health Insurance Corporation (Philhealth) Z Benefit Package (PZBP).

METHODS

A retrospective descriptive cohort study. A review of medical records was done from July 2017 to October 2023 to collect data and in-hospital outcomes of patients who underwent CABG surgery under Z benefit package.

RESULTS

One hundred twenty-six patients were included in the study. The mean age of patients was 60 years and majority of them were male and came from NCR. Hypertension was the leading cause of comorbidity. The top two most common in-hospital outcomes were hospital-acquired pneumonia and postoperative atrial fibrillation. Most commonly observed caused of increased length in hospitalization was pneumonia. The mean Society of Thoracic Surgeons (STS) (operative mortality) and Euro scores were 1.04 ± 0.82 and 0.88 ± 0.56, respectively. All patients had successful surgical outcome with no mortality and an average length of stay in the hospital of six days.

CONCLUSIONS

This study will serve as a future reference to enhance screening criteria and improved in-hospital outcomes for those who will undergo CABG under Z benefit package. The study also showed insights on clinical profile and in-hospital outcomes of patients who underwent CABG in our own institution and this may give way to a larger scale of study involving multiple centers who also offer the said program.

Human ; Coronary Artery Bypass ; Atrial Fibrillation ; Insurance, Health

The inflammatory nature of atherosclerosis has long been postulated, and though currently widely accepted, the concept is difficult to disseminate and to translate into concrete public health measures. Through the years, it has been discerned that low density lipoprotein (LDL) cholesterol serves as the stimulus for the inflammatory response when it is deposited into the subendothelium. LDL stimulates the migration of the inflammatory cells into the subendothelium; a sequelae of cellular immune responses and a cascade of cytokines ensue, eventually resulting in the formation of a vulnerable plaque. Inflammatory cells, particularly macrophages and lymphocytes, and their cytokines play a role in all stages of the atherosclerotic process, modulating the vascular remodeling process as more LDL cholesterol is absorbed into the subendothelial space and forms an ever enlarging lipid core. When inflammatory cells release metalloproteinases into the fibrous cap separating the lipid core from the lumen, plaque becomes vulnerable to rupture especially with increased shear stress from luminal blood flow resulting in thrombosis; clinically acute coronary syndromes become manifest. The role of mast cells, macrophage apoptosis, and the role of the vasa vasorum in plaque progression has recently been delineated. Pharmacologic intervention to aggressively lower LDL cholesterol culminated in the discovery of statins which were proven in large landmark trials to lower the morbidity and mortality associated with the atherosclerotic process. Several generations of statins have evolved; however, residual mortality is observed despite aggressive therapy. A recent trial showing the beneficial effects of statins in patients with acceptable or normal lipid profiles but with elevated high sensitivity C reactive protein (hsCRP) augurs a change in the paradigm of treatment for atherosclerosis. Inflammatory biomarkers such as hsCRP and lipoprotein-associated phospholipase A2 (Lp-PLA2) are anticipated to change guidelines and treatment algorithms, and public health policy. The implication of infectious processes as triggers of inflammation in the atherosclerotic process is also discussed, particularly the role of periodontal disease, the role of flu vaccination, and the role of bacteria such as Chlamydia and Helicobacter. 

Hydroxymethylglutaryl-coa Reductase Inhibitors ; Acute Coronary Syndrome ; C-reactive Protein ; Helicobacter ; Mast Cells ; Atherosclerosis ; Plaque, Atherosclerotic ; Immunity, Cellular ; Metalloproteases