Forty patients, 30 men and 10 women with an average age of 38.47 +/- 11.07 years, suffering from ankylosing spondylitis and attending a Rheumatology Outpatient Clinic, were evaluated for cardiovascular involvement. The evaluation was based on patients' clinical observation, electrocardiography, echocardiography, and chest x-ray. More than a simple review, this study was undertaken with the aim of arriving at a better clinical definition of the cardiovascular manifestations found in ankylosing spondylitis. In fact, of the 40 patients, 8 (20%) had systemic hypertension for which an explanation could not be found, 4 of whom were less than forty-five years old; the echocardiogram showed mitral valve prolapse in 4 patients (10%), 2 of them with a systolic murmur and other 2 with a protosystolic click on auscultation. More significant than the changes in conduction was the finding of a sinus bradycardia in 9 patients (22.5%), and a PR interval below 120 msec in 3 patients (7.5%). The authors conclude that the extension of cardiovascular changes in ankylosing spondylitis is more vast than usually acknowledged.

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In patients with a previous myocardial infarction, controversy exists regarding the significance of postexercise ST-segment elevation in the infarct-related leads. Although usually admitted to be a sign of left ventricular dysfunction or myocardial aneurysm, other studies however have related this finding to transient myocardial ischemia and to the presence of jeopardized but viable myocardium in the infarct area. The aim of the present study was to assess the significance of postexercise ST-segment elevation in Q-wave leads as a marker of transmural ischemia or left ventricular dysfunction in 36 consecutive patients, 16 with exercise-induced ST-segment elevation in infarct-related leads. Patients were evaluated by treadmill exercise testing, coronary angiography and ventriculography, thallium-201 tomographic scintigraphy and radionuclide ventriculography within 3 months of the first myocardial infarction. Sixteen patients (group I) had exercise-induced ST segment elevation and 20 (group II) postexercise inversion, no change or pseudonormalization of the T wave in infarct-related leads. The study showed no difference in infarct-related artery, vessel disease or luminal diameter stenosis in groups I and II. The overall agreement between ST shifts and myocardial perfusion in the infarct area was 30.56% with a κ coefficient of –0.33 (p = NS). The overall agreement between ST shifts and wall motion abnormalities was 69.44% with a κ coefficient of 0.39 (p < 0.01), stress-induced ST-segment elevation being associated with severe wall contractile disorders in 85% of the patients. In conclusion stress-induced ST-segment elevation in Q wave leads, although not a marker of wall motion abnormalities, is associated with akinesia or dyskinesia of the left ventricular wall.

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