• Title/Summary/Keyword: Left ventricular elastance

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Impact of Pulmonary Arterial Elastance on Right Ventricular Mechanics and Exercise Capacity in Repaired Tetralogy of Fallot

  • Soo-Jin Kim;Mei Hua Li;Chung Il Noh;Seong-Ho Kim;Chang-Ha Lee;Ja-Kyoung Yoon
    • Korean Circulation Journal
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    • v.53 no.6
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    • pp.406-417
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    • 2023
  • Background and Objectives: Pathophysiological changes of right ventricle (RV) after repair of tetralogy of Fallot (TOF) are coupled with a highly compliant low-pressure pulmonary artery (PA) system. This study aimed to determine whether pulmonary vascular function was associated with RV parameters and exercise capacity, and its impact on RV remodeling after pulmonary valve replacement. Methods: In a total of 48 patients over 18 years of age with repaired TOF, pulmonary arterial elastance (Ea), RV volume data, and RV-PA coupling ratio were calculated and analyzed in relation to exercise capacity. Results: Patients with a low Ea showed a more severe pulmonary regurgitation volume index, greater RV end-diastolic volume index, and greater effective RV stroke volume (p=0.039, p=0.013, and p=0.011, respectively). Patients with a high Ea had lower exercise capacity than those with a low Ea (peak oxygen consumption [peak VO2] rate: 25.8±7.7 vs. 34.3±5.5 mL/kg/min, respectively, p=0.003), while peak VO2 was inversely correlated with Ea and mean PA pressure (p=0.004 and p=0.004, respectively). In the univariate analysis, a higher preoperative RV end-diastolic volume index and RV end-systolic volume index, left ventricular end-systolic volume index, and higher RV-PA coupling ratio were risk factors for suboptimal outcomes. Preoperative RV volume and RV-PA coupling ratio reflecting the adaptive PA system response are important factors in optimal postoperative results. Conclusions: We found that PA vascular dysfunction, presenting as elevated Ea in TOF, may contribute to exercise intolerance. However, Ea was inversely correlated with pulmonary regurgitation (PR) severity, which may prevent PR, RV dilatation, and left ventricular dilatation in the absence of significant pulmonary stenosis.

Energetics of the Heart Model with the Ventricu1ar Assist Device

  • Chung, Chanil-Chung;Lee, Sang-Woo;Han, Dong-Chul;Min, Byoung-Goo
    • Journal of Biomedical Engineering Research
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    • v.17 no.1
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    • pp.43-48
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    • 1996
  • We investigated the energistics of the physiological heart model by comparing predictive indexes of the myocardial oxygen consumption (MOC), such as tension-time index (R), tension-time or force-time inteual (FTI), rate-pressure product (RPP), pressure-work index, and systolic pressure-volume area (PVA) when using the electro-hydraulic left ventricular device (LVAD). We developed the model of LVAD incorporated the closed-loop cardiovascular system with a baroreceptor which can control heart rate and time-varying elastance of left and right ventricles. On considering the benefit of the LVAD, the effects of various operation modes, especially timing of assistance, were evaluated using this coupled computer model. Overall results of the computer simulation shows that our LVAD can unload the ischemic (less contractile) heart by decreasing the MU and increasing coronary flow. Because the pump ejection at the end diastolic phase of the natural heart may increase the afterload of the left ventricle, the control scheme of our LVAD must prohibit ejecting at this time. Since the increment of coronary flow is proportional to the peak aortic pressure after ventricle contraction, the LVAD must eject immediately following the closure of the aortic valve to increase oxygen availability.

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Effects of vasopressin administration in the oral cavity on cardiac function and hemodynamics in rats

  • Fukami, Hayato;Sunada, Katsuhisa
    • Journal of Dental Anesthesia and Pain Medicine
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    • v.22 no.1
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    • pp.11-18
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    • 2022
  • Background: The vasoconstrictive effect of epinephrine in local anesthetics affects the heart, which leads to hesitation among dentists in injecting local anesthetics into patients with cardiovascular disease. Due to its vasoconstrictive effects, the present study investigated the effects of vasopressin administration on cardiac function in rats. Methods: Experiment 1 aimed to determine the vasopressin concentration that could affect cardiac function. An arterial catheter was inserted into the male Wistar rats. Next, 0.03, 0.3, and 3.0 U/mL arginine vasopressin (AVP) (0.03V, 0.3V, and 3.0V) was injected into the tongue, and the blood pressure was measured. The control group received normal saline only. In Experiment 2, following anesthesia infiltration, a pressure-volume catheter was placed in the left ventricle. Baseline values of end-systolic elastance, end-diastolic volume, end-systolic pressure, stroke work, stroke volume, and end-systolic elastance were recorded. Next, normal saline and 3.0V AVP were injected into the tongue to measure their effect on hemodynamic and cardiac function. Results: After 3.0V administration, systolic blood pressures at 10 and 15 min were higher than those of the control group; they increased at 10 min compared with those at baseline. The diastolic blood pressures at 5-15 min were higher than those of the control group; they increased at 5 and 10 min compared with those at baseline. The preload decreased at 5 and 10 min compared to that at baseline. However, the afterload increased from 5 to 15 min compared with that of the control group; it increased at 10 min compared with that at baseline. Stroke volume decreased at 10 and 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Stroke work decreased from 5 to 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Conclusion: Our results showed that 3.0 U/mL concentration of vasopressin resulted in increased blood pressure, decreased stroke volume and stoke work, decreased preload and increased afterload, without any effect on myocardial contractility.

Reproducibility of non-invasive measurement for left ventricular contractility using gated myocardial SPECT (게이트 심근 SPECT를 이용한 비침습적 심실 수축력 측정방법의 재현성)

  • Kim, Kyeong-Min;Lee, Dong-Soo;Kim, Yu-Kyeong;Cheon, Gi-Jeong;Kim, Seok-Ki;Chung, June-Key;Lee, Myung-Chul
    • The Korean Journal of Nuclear Medicine
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    • v.35 no.3
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    • pp.152-160
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    • 2001
  • Purpose: We tried to establish the reproducibility of the measurement of maximal elastance (Emax) and to compare the degree of the reproducibility of two estimation methods: single pressure-volume loop method and parameter optimization method. Materials and methods: In 47 patients (42 males and 5 females, $53{\pm}10$ years old) with suspected coronary artery disease (election fraction; 22-68%), gated Tc-99m MIBI myocardial SPECT and arterial tonometry were acquired. In 11 patients among these 47 patients, gated SPECT and tonometry were performed twice consecutively with patients in situ. Emax and void volume (Vo) were estimated using single pressure-volume loop method of Lee and parameter optimization method based on linear approximation of Yoshizawa. Correlation between the consecutive measurements by each method and correlation between the two estimation methods were compared. Results: Reproducibility of Emax (r=0.96) and Vo (r=0.99) by single pressure-volume method was better than the reproducibility of Emax (r=0.89) and Vo (r=0.64) by parameter optimization method. Correlations of Emax and Vo were fair between the two methods. The correlation of Emax (r=0.77) was better than that of Vo (r=0.55). Conclusion: Reproducibility of Emax measurement by single pressure-volume loop method using gated myocardial SPECT and arterial tonometry was excellent. Reproducibility by parameter optimization method was also fair but was less than that achieved by single pressure-volume method.

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