Pulmonary arterial hypertension in Saudi Arabia: Patients' clinical and physiological characteristics and hemodynamic parameters. A single center experience.

AIMS: The main objective of this study is to describe patients' clinical characteristics and physiological and hemodynamic parameters at the time of diagnosis in a pulmonary hypertension center in Saudi Arabia. MATERIALS AND METHODS: This study reports the results from a single pulmonary hypertension specialized center in Riyadh, Saudi Arabia, namely Prince Sultan Medical Military City/Cardiac Center (PSMMC & CC). Both newly diagnosed (incidence) and referred (prevalence) cases of pulmonary arterial hypertension are included. All characteristics, including clinical, physiological, and hemodynamic parameters at the time of diagnosis are described. RESULTS: A total of 107 patients were identified as having pulmonary arterial hypertension as diagnosed by right heart catheterization. The mean age at diagnosis was 36 (± 9) years, and there was a female preponderance of 62.6%. The mean duration between symptom onset and diagnosis was 27.8 (± 9.0) months. At the time of enrollment, 56.1% of patients were in functional class III and 16.8% were in functional class IV. Fifty five patients (51.4%) were diagnosed as idiopathic pulmonary arterial hypertension, 29 patients (27.1%) as congenital heart disease associated with pulmonary arterial hypertension, 16 patients (15.0%) as connective tissue diseases associated with pulmonary arterial hypertension, 4 patients (3.7%) as heritable pulmonary arterial hypertension, and 3 patients (2.8%) as portopulmonary hypertension. CONCLUSION: This data highlights the current situation of pulmonary arterial hypertension in Saudi Arabia. Our patients are much younger than patients described in other international registries but still detected as late in the course of the disease. A majority of patients displays severe functional and hemodynamic compromise.

Coronary vasospasm as a cause of angina following interventional recanalization.

Angina following a coronary intervention may be due to vasospasm rather than restenosis. Two cases of angina following a previously successful recanalization are described. In both cases vasospasm was documented as the cause of angina, determined in one case by using an ergonovine provocative test and in the other by using lesion response to nitroglycerine. Rather than another intervention, vasodilator treatment was instituted, with effective symptom amelioration.

Vascular endothelial platelet endothelial adhesion molecule-1 (PECAM-1) expression is decreased by TNF-alpha and IFN-gamma. Evidence for cytokine-induced destabilization of messenger ribonucleic acid transcripts in bovine endothelial cells.

Platelet endothelial cell-adhesion molecule-1 (PECAM-1, CD31) is constitutively expressed by vascular endothelium and concentrates at intercellular junctions. Regulation of PECAM-1 expression on endothelial cells may modulate leukocyte trafficking, angiogenesis, and vascular permeability. Given that cytokine activation induces profound alterations in endothelial phenotype, studies sought to determine whether cytokine treatment modulated PECAM-1 mRNA and protein content in macro- and microvascular endothelial cells. Northern blot analysis revealed expression of PECAM-1 mRNA transcripts in endothelial cells derived from bovine aorta, bovine glomeruli, and human umbilical vein under basal conditions. Treatment of endothelial cells with TNF-alpha and/or IFN-gamma led to dramatic decreases in steady-state levels of PECAM-1 mRNA transcripts. In contrast, reciprocal induction of ICAM-1 mRNA was evident. Actinomycin D chase experiments demonstrated that cytokines selectively destabilize PECAM-1 mRNA transcripts in bovine endothelial cells, decreasing the PECAM-1 mRNA transcript t1/2 from basal values of 15 +/- 2 h to 4 +/- 1 h in TNF-alpha- and IFN-gamma-treated cells (p < 0.005), an effect that appeared to be independent of new protein synthesis. Nuclear run-off analysis demonstrated no change in the rates of PECAM-1 gene transcription in response to cytokines treatment. Immunoblots and quantitative indirect immunofluorescence indicated decreased total cellular and cell-surface PECAM-1 protein expression following cytokine treatment. These findings provide evidence for cytokine-induced reciprocal regulation of transcripts of Ig-like adhesion molecules on vascular endothelium.