Left Ventricular Myocardial Oxygen Demand Research Articles

Left ventricular myocardial oxygen demand and subclinical dysfunction in patients with severe obesity referred for bariatric surgery

Background and aimsIncreased myocardial oxygen (O2) demand carries higher cardiovascular risk in hypertension. We hypothesized that myocardial O2 demand is increased in severe obesity and linked to early left ventricular (LV) dysfunction. Methods and resultsBaseline data from 106 severely obese subjects referred for gastric bypass surgery (42 ± 11 years, 74% women, body mass index [BMI] 41.9 ± 4.8 kg/m2, 32% with hypertension) in the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study was used. LV systolic function was assessed by biplane ejection fraction (EF), midwall shortening (MWS) and endocardial global longitudinal strain (GLS), and LV diastolic function by mitral annular early diastolic velocity (e’). Myocardial O2 demand was estimated from the LV mass-wall stress-heart rate product (high if > 1.62 × 106/2.29 × 106 g kdyne/cm2 bpm in women/men). High myocardial O2 demand was found in 33% and associated with higher BMI and high prevalence of low GLS (65%) and low MWS (63%) despite normal EF. In ROC analyses, higher myocardial O2 demand discriminated between patients with low vs. normal MWS and GLS (area under curve 0.71 and 0.63, p < 0.05). In successive multiple regression analyses, higher myocardial O2 demand was associated with lower LV MWS, GLS and average e’, respectively, independent of age, gender, BMI, pulse pressure, diabetes mellitus, and EF (all p < 0.05). ConclusionIn obese patients without known heart disease and with normal EF referred for bariatric surgery, high myocardial O2 demand is associated with lower myocardial function whether assessed by GLS or MWS independent of confounders. Clinicaltrials.gov identifierNCT01533142;

Cardioprotective effects of the Ιf current inhibition by ivabradine during cardiac dysfunction.

Heart rate is a fundamental determinant of cardiac function. Normally, the increase in heart rate is accompanied by increased cardiac function. But under pathological conditions such as myocardial infarction and heart failure, accelerated heart rate may become detrimental as it decreases the diastolic time for left ventricular filling and myocardial perfusion but increases left ventricular myocardial oxygen demand. Therefore, heart rate reduction is an appropriate strategy to protect cardiac function. Heart rate reduction can be achieved by different bradycardic drugs, including beta-blockers, calcium channel blockers and selective f-channel inhibitors. By competing with norepinephrine and epinephrine for binding sites, beta-blockers block beta-adrenoceptor-mediated responses to sympathetic stimulation. This induces heart rate reduction and negative inotropy. Calcium channel blockers block calcium influx via specific calcium channels, causing vasodilation and decreases in heart rate, conduction velocity within the heart and myocardial force generation. The selective f-channel inhibitor, ivabradine, inhibits If currents that play an exclusive role in pacemaking and thereby slows heart rate without altering myocardial inotropy. Since these drugs differ in their mechanisms of action, they may cause different beneficial and side effects and thus different outcome according to pathological states. After briefly describing the mechanisms involved in beta-blockers and calcium channel blockers, this review focuses on the bradycardic property of ivabradine and its pleiotropic actions.

Abstract 18780: Diminished Left Ventricular Myocardial Oxygen Demand During Dobutamine Stress Testing in the Elderly Reduces the Appearance of Inducible Wall Motion Abnormalities Indicative of Ischemia

Background: It has been observed that dobutamine stress may be less sensitive in the elderly and in those with LVH. We hypothesized that, in the elderly, a reduced increment in myocardial oxygen demand with dobutamine produces false negative results. Methods: We prospectively performed dobutamine cardiovascular magnetic resonance (DCMR) on 276 consecutively recruited individuals aged 55-85 years with risk factors for CAD. Rate pressure product (RPP), assessment of LV wall motion and volumes, aortic pulse wave velocity (PWV a measure of aortic stiffness) and first pass gadolinium enhanced LV perfusion defects (PD) indicative of ischemia were obtained on a 1.5T scanner at rest and after dobutamine infused to achieve 80% of the maximum predicted heart rate. Myocardial oxygen demand was assessed by the systolic pressure volume area (PVA), measured as LV stroke work (SW), [mean arterial pressure * stroke volume] plus potential energy [(1/2*end-systolic pressure) * end-systolic volume]}. All measures were assessed independently by personnel blinded to other data or participant identifiers. Differences were assessed with t-test; p &lt; 0.05 was significant. DCMR PD was considered as the gold standard for the detection of ischemia. Results: Participants averaged 68±8 years, were 80% white, 90% hypertensive, 43% diabetic and 55% men; all achieved target heart rate. With dobutamine, RPP increased 85% and LV end-diastolic volume index decreased. No subject had an inducible WMA without concomitant PD, but 28 had PD without inducible WMA (Table). In these false negatives, PVA was significantly lower (p= 0.03) and LVSW (p = 0.06) and PWV (p= 0.13) had strong trends toward being lower. The sensitivity of DCMR WMA for identifying PD indicative of ischemia was 33%. Conclusion: With dobutamine stress testing, the elderly had declines in LV preload and PVA. These findings provide a novel mechanistic explanation of why the elderly may have false negative wall motion during dobutamine stress.

Effects of Enhanced External Counterpulsation on Arterial Stiffness and Myocardial Oxygen Demand in Patients With Chronic Angina Pectoris

Enhanced external counterpulsation (EECP) is a noninvasive technique for treatment of symptomatic coronary artery disease in patients not amenable to revascularization procedures. However, the mechanisms underlying the benefits of EECP remain unknown. We hypothesized that decreases in arterial stiffness and aortic wave reflection are a therapeutic target for EECP. Patients with coronary artery disease and chronic angina pectoris were randomized (2:1 ratio) to 35 1-hour sessions of EECP (n = 28) or sham EECP (n = 14). Central and peripheral arterial pulse-wave velocity and aortic wave reflection (augmentation index) were measured using applanation tonometry before, and after 17 and 35 1-hour treatment sessions. Wasted left ventricular pressure energy and aortic systolic tension-time index, markers of left-ventricular myocardial oxygen demand, were derived from the synthesized aortic pressure wave. Exercise duration, anginal threshold, and peak oxygen consumption were measured using a graded treadmill test. Central arterial stiffness and augmentation index were decreased after 17 and 35 sessions in the treatment group. Measurements of peripheral arterial stiffness were decreased after 35 sessions in the treatment group. Changes in aortic pressure wave reflection resulted in decreased measurements of myocardial oxygen demand and wasted left ventricular energy. No changes in central or peripheral arterial stiffness were observed in the sham group. Furthermore, measurements of exercise capacity were improved in the EECP group but unchanged in the sham group. In conclusion, EECP therapy decreases central and peripheral arterial stiffness, which may explain improvements in myocardial oxygen demand in patients with chronic angina pectoris after treatment.

Changes in central artery blood pressure and wave reflection during a cold pressor test in young adults

The relative contribution of sympathetic nervous system (SNS)-induced increase in peripheral vascular resistance on central artery blood pressure (BP) and aortic wave reflection (augmentation index; AIx) is not completely understood. Central BP and wave reflection characteristics were measured using radial artery applanation tonometry before, during a 3-min cold pressor test (CPT), and 90 and 180-s post-CPT in 15 young, healthy adults (25 +/- 1 years). The CPT resulted in a greater magnitude of change in the estimated aortic systolic (31 vs. 23%, P < 0.05) and pulse (31 vs. 13%, P < 0.05) BP compared with the change in brachial artery BP. Additionally, the CPT resulted in an increased mean arterial pressure (MAP) (P < 0.05) and AIx (10 +/- 2 vs. 26 +/- 2%, P < 0.05). The change in MAP during the CPT was correlated to the change in AIx (r = 0.73, P < 0.01) and inversely related to roundtrip duration of the reflected wave to the periphery and back (r = -0.57, P < 0.05). The present study suggests that cold pressor testing results in a significant increase in arterial wave reflection intensity, possibly due to an increased MAP. However, the greater increase in systolic and pulse BP in the central compared with the peripheral circulation suggests that increased central artery wave reflection intensity contributes to increased left ventricular myocardial oxygen demand during CPT-induced hypertension.

Arterial-Wave Reflections Are Increased in Heart Failure Patients With a Left-Ventricular Assist Device

Chronic heart failure (HF) is associated with increased central arterial pulse-wave reflections, which may contribute to increased myocardial oxygen demand. Although the treatment of HF via left-ventricular assist device (LVAD) placement has recently become widespread, the effects of LVAD therapy on central arterial pulse-wave reflections are unknown. Central aortic pulse-wave analysis was performed on patients with end-stage HF awaiting cardiac transplantation and on healthy age-matched controls using the SphygmoCor (Akor Medical, Sydney, Australia) system. Arterial pulse-wave data were compared between patients receiving LVAD support versus those receiving intravenous inotropic drugs and healthy control patients. Five patients on LVAD support were compared with 10 patients on inotropic drugs and 10 healthy control patients. Aortic augmented pressure and the aortic augmentation index (AI(a)) were higher in LVAD patients compared with inotrope and control patients, despite similar brachial and aortic blood pressures between groups. The AI(a) was significantly higher in LVAD patients than in patients on inotropic drugs (28.2% +/- 10% v 7.9% +/- 9%, P < or = .01). Additionally, there was a significantly higher aortic systolic tension time index, an index of left-ventricular myocardial oxygen demand, in the LVAD group compared with the inotrope group (2655 +/- 298 mm Hg/sec/min v 1748 +/- 303 mm Hg/sec/min, P < .01). Central arterial pressure-wave reflection is increased in end-stage HF patients on LVAD support compared with those on inotropic drugs, leading to an increase in aortic augmented pressure, AI(a), and systolic tension time index. The AI(a) is also higher in LVAD patients than in healthy controls. This increased central arterial-wave reflection places an additional hemodynamic load on the LVAD device and may have relevance to the medical management of patients after LVAD placement and to the longevity of the LVAD device itself.

Reduction of left ventricular epicardial segment length by 100% oxygen breathing in open-chest dogs.

We conducted this study in order to learn whether or nt oxygen inhalation reduces left ventricular size, one of the major determinants of myocardial oxygen demand. In 11 open-chest dogs, a Mercury-in-Silastic gauge was applied to measure left ventricular circumferential length while the dogs were being ventilated with either room air or 100% oxygen. Four characteristic notches were identified on the resulting length curve: L1, length at the beginning of ejection; L2, length at the end of ejection; L3, length in early diastole; and L4, length at end diastole, L1 was shortened from 24.9 +/- 10.5 to 24.4 +/- 9.9 mm (a decrease of 1.4 +/- 2.1%) by oxygen breathing, L2 was also shortened from 26.8 +/- 11.5 to 26.2 +/- 10.7 mm (a decrease of 1.5 +/- 2.9%), L3 from 17.5 +/- 4.4 to 17.4 +/- 4.3 mm (a decrease of 0.7 +/- 2.7%) and L4 from 17.7 +/- 4.8 to 17.5 +/- 4.7 mm (a decrease o 1.3 +/- 2.4%). These changes all disappeared when the inspiratory gas was changed from oxygen back to air. Heart rate and left ventricular end-diastolic pressure showed no significant changes but were accompanied by a slight reduction in aortic pressure and myocardial contractile force. This study demonstrated a small but consistent reduction in left ventricular circumferential length by oxygen breathing. This reduction in left ventricular size will reduce left ventricular tension and thus result in reduction of left ventricular myocardial oxygen demand when oxygen inhalation is applied to patients with ischemic heart disease.