Mechanisms of exercise-induced ST-segment depression in patients without typical angina pectoris.
OBJECTIVE
To evaluate if exercise-induced ST-segment depression without typical angina pectoris is related to increases in sympatho-adrenal activity or beta-adrenoceptor sensitivity.


METHODS
Thirteen patients (four men) aged 35-62 years with ST-segment depression during exercise but atypical symptoms and normal myocardial scintigraphy, and 13 matched controls.


METHODS
Patients and controls were compared regarding responses with: (i) exercise testing without treatment, (ii) exercise testing following beta-adrenoceptor blockade by propranolol (0.15 mg kg(-1) i.v.), (iii) incremental adrenaline infusions (0.1, 0.2, 0.4 and 0.8 nmol kg(-1) min(-1)) and (iv) adrenaline infusions during alpha-adrenoceptor blockade by phentolamine (0.5 mg min(-1)).


METHODS
ST-segment depression and tissue Doppler parameters reflecting contractility.


RESULTS
Exercise lowered the ST-segment by 2.44 mm without and 0.87 mm with beta-adrenoceptor blockade (P < 0.001 for difference) amongst patients, but not amongst controls. Maximal heart rate was slightly higher amongst patients (P < 0.05), despite similar loads and plasma catecholamine responses to exercise in the two groups; this difference disappeared after beta-adrenoceptor blockade with propranolol. ST-segment depression during adrenaline infusion was greater in patients compared with controls (P < 0.01) despite similar increases in heart rate. alpha-Blockade enhanced the ST-segment depression (P < 0.001) and heart rate (P < 0.001) responses to adrenaline infusion more markedly amongst patients. Tissue Doppler imaging showed similar contractility and diastolic relaxation responses of patients and controls to adrenaline, but early diastolic movements did not increase amongst patients after phentolamine (P < 0.01).


CONCLUSIONS
Exercise-induced ST-segment depression in patients with a low likelihood of ischaemic heart disease is related to increased beta-adrenergic sensitivity regarding chronotropic and electrophysiological, but not inotropic responses.
Sundkvist
G M G
GM
Division of Clinical Physiology, Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden.
Hjemdahl
P
P
Kahan
T
T
Melcher
A
A
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000328:Adult; D001145:Arrhythmias, Cardiac / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D018618:Echocardiography, Doppler, Color; D004562:Electrocardiography / Q000187:drug effects; D004837:Epinephrine; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006321:Heart / Q000000981:diagnostic imaging; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D019275:Radiopharmaceuticals; D017256:Technetium Tc 99m Sestamibi; D015899:Tomography, Emission-Computed, Single-Photon
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D019275:Radiopharmaceuticals; D017256:Technetium Tc 99m Sestamibi; D011433:Propranolol; D004837:Epinephrine; D010646:Phentolamine