Invasive and noninvasive assessment of exercise-induced ischemic diastolic response using pressure transducers

Abstract

Left ventricular (LV) pressure curve shows early high-magnitude changes in the presence of induced ischemia. A dramatic rise in LV and left atrial end-diastolic pressures occurs within seconds to minutes in the presence of ischemia induced by dynamic or handgrip exercise as well as pacing of 38 to 183% and during short coronary balloon occlusion of 32 to 208% of baseline. Changes in relaxation or volumetric filling rate or ejection fraction were significantly less pronounced. Similar end-diastolic abnormalities occurring mainly in patients with coronary artery disease (CAD) have been shown in noninvasive recordings obtained by pressure transducer placed over the point of maximal LV beat (pressocardiograms). Specifically, the amplitude of the A wave to total excursion of pressocardiogram showed a similar high-magnitude increase after dynamic or handgrip exercise in average by 60 to 142% of baseline; however, changes in pressocardiographic relaxation time indexes were only slightly abnormal. A well-defined "ischemic pattern" of pressocardiographic diastolic changes with handgrip, showed a high prevalence in CAD patients. The assessment of diastolic changes in the presence of handgrip-inducible ischemia using noninvasive pressure transducers might provide after further studies a simple complementary diagnostic tool to assist in identification of patients with atypical or asymptomatic CAD.

Fig. (1)

Left ventricular and aortic high-fidelity pressure curves in a healthy subject (A) and in a patient with coronary disease (B). AoP= aortic pressure; dP/dt = first derivative of left ventricular pressure; EDP = left ventricular end-diastolic pressure; LVP = left ventricular pressure. TORET =total relaxation time. Handgrip leads in A to a small decrease of end-diastolic pressure from 8 to 6 mmHg. In contrast, there is a dramatic EDP rise in B from 26 to 41 mmHg - increase by 58%(modified Krayenbuehl HP, Eur J Cardiol 1974).

Fig. (2)

Simultaneous high-fidelity recordings of aortic (AoP) and left ventricular (LVP) pressures as well as of pressocardiogram (Presso) and external phonocardiogram (PCG) and electrocardiogram lead II (ECG). The onset of systolic onset (C points) and the lowest diastolic (0 Points) are identical and the slopes of both curves similar. The first derivatives of LVP and presso (LV dP/dt and Presso dP/dt, respectively) show a very similar configuration. The low end-diastolic pressure corresponds to normal A wave (A) to total height (H) of Presso and the TORET of LVP and Presso curves is identical (Personal archive).

Fig. (3)

Simultaneous high-fidelity recordings of left ventricular pressure and left atrial pressure (LAP) -both obtained by micromanometerand pressocardiogram in a patient with dyspnea on effort and severe diastolic dysfunction of the left ventricle. All high-fidelity pressure transducer-derived curves are obtained by identical pressure transducers (micromanometers in left ventricle and left atrium as well as strain gage external pressure transducer externally). There is a temporal coincidence of the onset of systolic upstroke point (C points of both curves) and an only 9 ms time difference in the lowest points of pressocardiographic and LVP curves. The greatly increased LVEDP/LAP of 45 mmHg is reflected in pressocardiogram by corresponding greatly increased A wave (A/H =40%), whereas the total relaxation time of left ventricular pressure and pressocardiogram is only slightly prolonged. C = onset of systolic upstroke of both left ventricular and pressocardiogram; LAP= Left atrial pressure; LAPa = A wave of LAP. Other abbreviations as in (Personal archive from Univ. of Zurich).

Fig. (4)

Healthy subject showing a “Normal diastolic response”: Simultaneous recordings of electrocardiogram (ECG), PCG (medium and low frequencies) and pressocardiogram (Presso) at rest and during handgrip. All variables are at rest and during handgrip within normal limits with a shortening of TORET and no change in A/H with handgrip exercise. The A/H and TORET are increasing, but remain within normal limits. HR = heart rate; R-type = relaxation type; TORETI = total relaxation index. Other abbreviations as in (Fig. 2).

Fig. (5)

a: Asymptomatic patient with hypertension showing a “positive presso test” result and a “non-ischemic diastolic response” of Relaxation (R) -type. TORET is slightly increased at rest. Both TORET and A/H are slightly increasing and TORETI decreasing with handgrip. b: Asymptomatic patient with hypertension showing a “non-ischemic diastolic pattern” of Compliance (C )-type. All indexes are within normal limits at rest. During handgrip, TORET is shortened and A/H is slightly abnormal. Abbreviations as in (Figs. 2 and 3).

Fig. (6)

Pressocardiogram from an asymptomatic 67-year-old man at rest, A/H is slightly increased and TORETI slightly decreased (mixed or RC-type). At handgrip 1 min and 2 min, there is a dramatic increase of A/H (HG1 at 56%and HG2 at 64%of baseline) and a decrease of TORET and TORETI increase. The automated evaluation shows the presence of a “positive” presso test with “severe LV diastolic dysfunction” at exercise and an “RC-type” at rest and “C-type” at exercise as well as a “deterioration of type” due to “RCàC” change resulting to the diagnosis of “ischemic” pattern. Subsequent CTCA showed multiple calcified “mixed” plaques in all coronary vessels without significant stenoses of >50%. Same abbreviations as in (Figs. 2 and 3).

Fig. (7)

Hypertensive patient with dyspnea on effort –NYHA II showing normal findings at rest and severe diastolic abnormalities with handgrip with a typical “ischemic diastolic response” of compliance type. At rest all indexes are within normal limits. During 1 and 2 min of handgrip, A/H is increased at 314%and 264%over the baseline value, respectively. Thus, the dyspnea on effort is most probably caused by significant ischemia with associated dramatic increase in LV filling pressures. Abbreviations as in (Figs. 3 and 4).