Elevated left ventricular filling pressure during angina.

catheterization procedures. We present a left ventricular (LV) pressure recording from a patient with coronary artery disease (CAD), who developed angina following coronary angiography with marked raise in left ventricular end-diastolic pressure (LVEDP) which normalized after sublingual nitroglycerin. A 50-year-old male hypertensive presented with exertional angina. Clinical examination, electrocardiogram, and echocardiogram were normal including normal left ventricular systolic and diastolic function. Diagnostic coronary angiogram was done using nonionic contrast that showed severe double vessel CAD. Pigtail catheter was introduced into the LV prior to LV angiogram. The LV pressure was 140/8 mmHg. The patient then started to complain of severe chest pain with monitor leads showing ST depression with no change in heart rate. The LV pressure recording was done during angina and showed markedly elevated LVEDP (40 mmHg, Figure 1). He was immediately given 2 puffs of sublingual nitroglycerin spray (0.8 mg) for the relief from angina. The LV pressure recording showed normalization of LVEDP (7 mmHg, Figure 2). Pacing-induced and coronary occlusion-induced experimental ischemia studies have demonstrated raise in LVEDP during myocardial ischemia.1,2 Acute myocardial ischemia causes elevated LVEDP due to an increase in the stiffness of the LV and subsequent diastolic dysfunction.1,2 Studies have demonstrated that ischemia causes asynchrony in regional filling leading to delayed filling of the ischemic myocardial segment with delayed and incomplete left ventricular relaxation and wall motion contractility along with loss of elastic recoil and thus increasing the chamber stiffness. Exerciseinduced ST depression is caused by subendocardial ischemia due to increased LVEDP. Nitroglycerin reduces LV pre-load, afterload, and myocardial wall tension, favouring redistribution of flow to the subendocardial myocardium. Furthermore, nitroglycerin has vasodilatory effect, increasing coronary flow to hypoperfused regions and flow through collaterals.