Association of chest pain versus dyspnea as presenting symptom for coronary angiography with demographics, coronary anatomy, and 2-year mortality
INTRODUCTION/BACKGROUND:The association of chest pain versus dyspnea with demographics, coronary angiographic findings, and outcomes of patients undergoing coronary angiography is unknown. MATERIAL AND METHODS/METHODS:We studied 1,053 patients who had coronary angiography to investigate the association of chest pain versus dyspnea with demographics, coronary angiographic findings, and outcomes. RESULTS:Of 1,053 patients, 654 (62%) had chest pain, 229 (22%) had dyspnea, and 117 (11%) had chest pain and dyspnea. Patients with dyspnea were older (p < 0.0001) and had higher serum creatinine (p = 0.0011), lower left ventricular ejection fraction (LVEF) (p < 0.0001), more cardiogenic shock (p = 0.0004), less obstructive coronary artery disease (CAD) (p < 0.0001), less percutaneous coronary intervention (p < 0.0001), and similar 2-year mortality. Stepwise Cox regression analysis showed no significant difference in mortality between chest pain and dyspnea. Significant risk factors for time to death were age (hazard ratio (HR) = 1.07, p < 0.0001), serum creatinine (HR = 1.5, p < 0.0001), body mass index (HR = 0.93, p = 0.005), and obstructive CAD graft (HR = 3.2, p = 0.011). CONCLUSIONS:Patients undergoing coronary angiography presenting with dyspnea were older and had higher serum creatinine, lower LVEF, more frequent cardiogenic shock, less obstructive CAD, and less percutaneous coronary intervention compared to patients presenting with chest pain but similar 2-year mortality.
Vascular Ehlers-Danlos syndrome: pathophysiology, diagnosis, and prevention and treatment of its complications
The Ehlers-Danlos syndrome consists of a group of inherited connective tissue disorders caused by defects in the synthesis of collagen. The vascular type 4 form of Ehlers-Danlos syndrome (VEDS) is associated with serious vascular complications in young adults, such as the spontaneous rupture of large-caliber and medium-caliber arteries, often without true aneurysm formation or dissection. VEDS is inherited as an autosomal dominant trait that is caused by mutations in the COL3A1 gene. It affects the synthesis and structure of the pro a1 (III) chain of collagen type III, which causes vascular wall weakness. The diagnosis of VEDS is made from major and minor clinical criteria and can be confirmed by abnormalities in procollagen production and molecular genetic testing. Recently, the results of a study using the b-blocker celiprolol demonstrated a reduction in vascular complications of VEDS. The mechanisms of benefit may be related to a reduction in vascular hemodynamic stress with exercise and/or through a reduction in transforming growth factor-b. Inhibitors of the renin-angiotensin system may also be beneficial in VEDS. Surgery may be beneficial in treating the complications of VEDS.