Frequency potentiation and postextrasystolic potentiation in patients with and without coronary arterial disease.

Abstract

Frequency potentiation and postextrasystolic potentiation of myocardial contractility were induced in 17 patientsfound not to have cardiac disease (group i) and in Io patients with coronary arterial disease (group 2). Atrial stimulation was performed starting at a rate of IoI/min and going up to 200/nin (frequency potentiation). Single, premature ventricular beats with decreasing coupling intervals were induced everyfifteenth beat during basal atrial stimulation at 2s/min, after which compensatory pauses were provided (postextrasystolic potentiation). The time derivative of left ventricular pressure (dp/dt) was used as an index of contractility. With increasing heart rate dp/dt max was augmented equally, in bothgroups ofpatients, byfrequency increases and premature beats (the coupling interval of the extrasystole being expressed as heart rate). dp/dt min and left ventricular systolic pressure remained unchanged while left ventricular end-diastolic pressure decreased in bothgroups ofpatients with the twoforms ofpotentiation. It was concluded that both theseforms ofpotentiation have the same augmenting effect on myocardial contractility. Shortening the coupling intervals of premature beats caused a decrease in left ventricular end-diastolic pressure, suggesting that the Frank-Starling mechanism was not involved in postextrasystolic potentiation. Patients with coronary arterial disease had lower values of dp/dt max, dp/dt min, and higher values of left ventricular end-diastolic pressure during rest and stimulation procedures, while the systolic pressures equalled those in the control group. Though individual case values from the healthy and diseased hearts might be similar, it was only under the stress ofpotentiation that the true state of contractility was made apparent. Impairment of dp/dt min was not found without an impairment of dp/dt max in the presence of myocardial ischaemia.

Influence of heart rate increase on uncorrected pre-ejection period/left ventricular ejection time (PEP/LVET) ratio in normal individuals.

“…It is probable that the PEP is prevented from Results lengthening during the tachycardia-induced decrease in stroke volume by a compensatory shorten-Under basal conditions the systolic time interval ing through the increased contractility associated values in our subjects were within the accepted with tachycardia (Vatner and Braunwald, 1974;normal range (Table). With increase of the basal Schwarz, Thormann, and Winkler, 1975;Roy, heart rate from 73-94±1-97 to 103.61±2-72/min, Sowton, and DiLuzio, 1975). there was a consistent shortening of the QS2 and…”

Mechanics of postextrasystolic potentiation in normal subjects and patients with valvular heart disease.

“…All patients were in sinus Left heart catheterization was performed in a retrograde fashion rhythm and the QRS duration did not 300 900 625 400 1100 800 450 1050 515 500 1050 725 410 1000 850 550 1500 1040 475 1350 960 485 1360 1120 490 1310 890 625 910 1055 469 1153 858 88 210 196 490 1050 740 465 960 725 500 1100 815 470 950 800 635 1140 940 600 1270 1100 527 1078 853 72 120 143 475 1150 790 425 1275 850 500 1275 815 565 1340 950 550 910 935 480 1310 885 575 1500 1060 550 1175 770 515 1242 882 53 172 97 550 1115 925 590 1050 855 310 1140 650 548 1278 930 460 900 685 550 1075 835 550 1375 975 508 1133 836 96 155 Dynamic wall thickness was computed for all frames subsequent to end-diastole assuming a constant mass for each frame, according to the method of Hugenholtz. 5 Briefly, iteration...…”