Karel Zeman

Amlodipine in patients with stable angina pectoris treated with nitrates and beta-blockers. The influence on exercise tolerance, systolic and diastolic functions of the left ventricle

The effects of 5 and 10 mg of amlodipine and of placebo were compared in 21 patients with stable angina pectoris and multivessel coronary artery disease. The blind comparison was performed by means of bicycle ergometry and stress echocardiography using esophageal stimulation of the left heart atrium. All patients subsequently received placebo, amlodipine 5 mg and 10 mg for 2 weeks. In bicycle ergometry both doses of amlodipine in comparison with placebo significantly lowered the ST segment depression in lead V5 and prolonged the time to onset of angina. The exercise duration was significantly prolonged only after 10 mg of amlodipine. In stress echocardiography 10 mg of amlodipine significantly improved ejection fraction and reduced wall motion score during stimulation and increased peak velocity of relaxation of left ventricular posterior wall at rest and immediately after stimulation. In the patients with left ventricular end-diastolic pressure < or = 20 mmHg, amlodipine reduced the ratio of peak transmitral flow velocity in atrial contraction to that in early diastole (A/E) at rest and shortened deceleration time at rest and immediately after stimulation. Amlodipine in patients with stable angina pectoris significantly improved the exercise tolerance and the function of the left ventricle in a dose-dependent way. Amlodipine was well tolerated.

Time-frequency interpretation of ultra-high-frequency QRS components

This paper presents a method for time-frequency representation of ultra-high-frequency components in the QRS complex in high-sensitivity and high-frequency electrocardiography signal measurement. Time-frequency interpretation forms shapes that look like fire - FLAMES. The width, intensity and position of FLAMES characterise the electrical properties of the human heart. FLAMES are able to differentiate electrical changes during asynchronous heart muscle activation and identify changes in electrical activation during heart ischemia, infarctions and structural changes of the myocardium. The difference in FLAMES is demonstrated in healthy young subject and heart-failure subject.