Influence of critical closing pressure on systemic vascular resistance and total arterial compliance: A clinical invasive study

Background: A prolonged corrected QT (QTc) interval is a known risk factor for adverse cardiac events. Understanding the determinants and physiologic correlates of QTc is necessary for selecting proper strategies to reduce the risk of adverse events in high-risk patients. We sought to evaluate the role of arterial stiffness in heart failure as a determinant of QTc prolongation. Method: This was an observational study that recruited ambulatory heart failure patients (New York Heart Association Classes I–II) from an outpatient heart failure clinic. In the supine resting position, consented patients underwent noninvasive 12-lead electrocardiograph (ECG) and hemodynamic monitoring using BioZ Dx impedance cardiography. ECGs were evaluated by a reviewer blinded to clinical data, and QTc interval was automatically computed. Patients with pacing or bundle branch block (BBB) were analyzed separately. Strengths of associations were evaluated using Pearson’s r coefficients and multivariate linear regression. Results: The final sample ( N = 44) was 62 ± 13 years of age and 64% male with ejection fraction of 34% ± 12%. At univariate level, QTc interval moderately ( r > .50) correlated with cardiac output, left cardiac work index, systemic vascular resistance, and total arterial compliance in patients with intrinsically narrow QRS complexes. At the multivariate level, increasing systemic vascular resistance and decreasing total arterial compliance remained independent predictors of widening QTc interval in this group ( R2 = .54). No significant correlations were seen in patients with pacing or BBB. Conclusions: In the absence of conduction abnormalities, magnitude of arterial stiffness, an indirect measure of endothelial dysfunction, is associated with QTc interval prolongation.

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Distinct Contribution of Systemic Blood Flow to Hypertension in an African Population Across the Adult Lifespan

Hypertension ◽

10.1161/hypertensionaha.120.14925 ◽

2020 ◽

Vol 76 (2) ◽

pp. 410-419

Author(s):

Angela J. Woodiwiss ◽

Keneilwe N. Mmopi ◽

Vernice Peterson ◽

Carlos Libhaber ◽

Hamza Bello ◽

...

Keyword(s):

Blood Pressure ◽

Stroke Volume ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Pulse Pressure ◽

Arterial Compliance ◽

African Ancestry ◽

Systemic Blood Flow ◽

Age Related ◽

Total Arterial Compliance

Although hypertension in groups of African ancestry is volume-dependent, the relative impact of systemic flow (stroke volume, peak aortic flow [Q]) versus vascular mechanisms (systemic vascular resistance, aortic characteristic impedance [Zc], total arterial compliance) components of arterial load has not been evaluated across the adult age range. In participants of African ancestry (n=824, age=16–99 years, 68.3% female), using central arterial pressure and aortic velocity and diameter measurements in the outflow tract, we determined the hemodynamic correlates of age-related increases in blood pressure. Strong independent positive relations between age and stroke volume or peak aortic Q were noted ( P <0.0001), effects associated with ventricular end diastolic volume and aldosterone-to-renin ratios. Age-related increases in mean arterial pressure were associated with stroke volume and not systemic vascular resistance. Although age-Q relations began from early adulthood, initially an inverse association between age and aortic Zc ( P <0.0001) driven by increments in aortic root diameter ( P <0.0001) prevented an enhanced systolic blood pressure and pulse pressure. When Zc began to positively relate to age ( P <0.0001), age-Q relations translated into increases in forward wave pressures and hence systolic blood pressure and pulse pressure. Age relations with pulse pressure were as strongly determined by Q as by Zc or total arterial compliance (0.027±0.001 versus 0.028±0.001 and 0.032±0.003 mm Hg per yearly increase in pulse pressure produced by Q, Zc, and total arterial compliance; P <0.0001). Uncontrolled hypertension (confirmed with 24-hour blood pressure) was determined more by Q, Zc, and total arterial compliance than by increases in systemic vascular resistance ( P <0.0005 for comparison). In conclusion, relationships between age and systemic blood flow contribute markedly to hypertension in groups of African origins.

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Contribution of systemic vascular resistance and total arterial compliance to effective arterial elastance in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00823.2002 ◽

2003 ◽

Vol 285 (2) ◽

pp. H614-H620 ◽

Cited By ~ 85

Author(s):

Denis Chemla ◽

Isabelle Antony ◽

Yves Lecarpentier ◽

Alain Nitenberg

Keyword(s):

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Arterial Compliance ◽

Aortic Pressure ◽

Left Ventricular ◽

Reliable Estimate ◽

Arterial Elastance ◽

Total Arterial Compliance ◽

Arterial Load ◽

Effective Arterial Elastance

The respective contribution of systemic vascular resistance ( R) and total arterial compliance ( C) to the arterial load remains to be established in humans. Effective arterial elastance ( Ea), i.e., the left ventricular end-systolic pressure (LVESP)-over-stroke volume ratio, is a reliable estimate of arterial load. It is widely accepted that Ea mainly relates to mean aortic pressure (MAP) and thus to the R-to- T ratio ( R/ T ratio), where T is cycle length. We tested the contribution of R/ T and 1/ C to Ea in 20 normotensive and 46 hypertensive subjects (MAP range: 84–160 mmHg). The multilinear model applied ( Ea = 1.00 R/ T + 0.42/ C – 0.04; r2 = 0.97). The sensitivity of Ea to a change in R/ T was 2.5 times higher than to a similar change in 1/ C in both normotensive and hypertensive adults. The LVESP was more strongly related to systolic aortic pressure (SAP; r2 = 0.94) than to MAP ( r2 = 0.83), and LVESP matched 90% SAP (bias = 0 ± 5mmHg). An alternative model of Ea is proposed, in which Ea is proportional to the heart rate × SAP product-over-cardiac index ratio whatever the MAP.

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A square-pulse flow method for measuring characteristics of the arterial bed

Journal of Applied Physiology ◽

10.1152/jappl.1976.40.3.425 ◽

1976 ◽

Vol 40 (3) ◽

pp. 425-433 ◽

Cited By ~ 3

Author(s):

M. G. Bottomley ◽

G. W. Mainwood

Keyword(s):

Arterial Compliance ◽

Peripheral Resistance ◽

Mean Value ◽

Pressure Response ◽

Arterial System ◽

Response Curves ◽

Arterial Tree ◽

Pulse Flow ◽

Critical Closing Pressure ◽

Closing Pressure

A device was designed to provide a “square” pulse of blood flow into the arterial system. Pulses were injected into the carotid artery of the rabbit during transient cardiac arrest. Analysis of pressure response curves generated by the flow provides information as to the state of the arterial tree. With certain assumptions it is possible to estimate from these curves lumped values of peripheral resistance, critical closing pressure, and arterial compliance. In a series of 12 rabbits the mean value of peripheral resistance was found to be 0.21 +/- 0.7 mmHg-ml-1-min and critical closing pressure was estimated to be 23.6 +/- 3.8 mmHg. This method gives two possible values for arterial compliance 0.036 +/- 0.010 and 0.055 +/- 0.010 ml-mm-1 based, respectively, on the rise and decay curves of the pressure response. The theory and limitations of the method are discussed. The use of the method is illustrated in following the response to increased PCO2 and hemorrhage.

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Relaxin Modifies Systemic Arterial Resistance and Compliance in Conscious, Nonpregnant Rats

Endocrinology ◽

10.1210/en.2003-1612 ◽

2004 ◽

Vol 145 (7) ◽

pp. 3289-3296 ◽

Cited By ~ 93

Author(s):

Kirk P. Conrad ◽

Dan O. Debrah ◽

Jackie Novak ◽

Lee A. Danielson ◽

Sanjeev G. Shroff

Keyword(s):

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Therapeutic Potential ◽

Muscle Tone ◽

Arterial Compliance ◽

Renal Arteries ◽

Conscious Rat ◽

Systemic Hemodynamic ◽

Arterial Load ◽

Passive Mechanics

Abstract Relaxin emanates from the corpus luteum of the ovary and circulates during pregnancy. Because the hormone is a potent renal vasodilator and mediates the renal vasodilation and hyperfiltration of pregnancy in conscious rats, we reasoned that it might also contribute to the broader cardiovascular changes of pregnancy. We began investigating this concept by testing whether relaxin can modify systemic arterial hemodynamics and load when chronically administered to nonpregnant rats. The major objectives of the present work were to determine whether relaxin administration to nonpregnant rats 1) modifies cardiac output (CO), systemic vascular resistance, and global arterial compliance (AC), and 2) regulates the passive mechanics of isolated arteries. To accomplish the first objective, we developed a conscious rat model for assessment of global AC. Passive mechanics of small renal arteries were assessed using a pressure arteriograph. Chronic administration of recombinant human relaxin by sc osmotic minipump to conscious, female, nonpregnant rats reduced the steady arterial load by decreasing systemic vascular resistance, increased CO, and reduced the pulsatile arterial load by increasing global AC as quantified by two indices—AC estimated from the diastolic decay of aortic pressure and CO and AC estimated by the ratio of stroke volume-to-pulse pressure. In another group of rats, relaxin administration also regulated the passive mechanics of small renal arteries, indicating that, in addition to reduction in vascular smooth muscle tone, modification of the vascular structure (e.g. extracellular matrix) contributes to the increase in global AC. These findings suggest a role for relaxin in the systemic hemodynamic changes of pregnancy, as well as novel therapeutic potential for relaxin in modifying arterial stiffness and cardiac afterload.

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Effect of Beta-adrenergic Blockade on Elevated Arterial Compliance and Low Systemic Vascular Resistance in Cirrhosis

Scandinavian Journal of Gastroenterology ◽

10.1080/00365520120440 ◽

2001 ◽

Vol 36 (6) ◽

pp. 653-657

Author(s):

S. Møller, F. Bendtsen, J. H. Henri

Keyword(s):

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Arterial Compliance ◽

Adrenergic Blockade ◽

Beta Adrenergic

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Abstract 15631: The Hemodynamic Determinants and Physiologic Correlates of QTc Interval Using Impedance Cardiography in Heart Failure

Circulation ◽

10.1161/circ.132.suppl_3.15631 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Fadi Khraim ◽

Rodolfo Pike ◽

Jennifer Williams ◽

Salah S Al-Zaiti

Keyword(s):

Heart Failure ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Impedance Cardiography ◽

Arterial Compliance ◽

Qtc Interval ◽

Cardiac Events ◽

Heart Failure Patients ◽

Qrs Duration ◽

Duration Effect

Background: Prolonged QTc interval is a known risk factor for adverse cardiac events, including sudden and non-sudden cardiac death. Understanding the determinants and physiologic correlates of QTc can guide the proper strategy for the primary prevention of sudden death in high risk patients. Methods & Results: This was an observational study that recruited ambulatory heart failure patients (NYHA I-III) from an outpatient clinic in NL, Canada. In supine resting position, consented participants underwent non-invasive 12-lead ECG and hemodynamic monitoring using BioZ Dx Impedance Cardiography (Sonosite Inc., WA, USA). ECGs were evaluated by a reviewer blinded to clinical data. Participants with pacing (n=12) or left bundle branch block (n=9) were excluded. Three measures of interest were automatically computed: (1) QTc interval (i.e., from QRS onset to T offset), (2) QRS duration (i.e., from QRS onset to QRS offset), and (3) JTc (i.e., QTc interval minus QRS duration). Effect sizes were computed using Pearson’s r coefficients. The final sample (n=23) was 62±13 years of age and 70% male with LVEF of 34±10%. The mean QTc was 441±39 milliseconds, and 10 patients (43%) had prolonged QTc (≥450 milliseconds). QTc interval negatively correlated with cardiac output (r= -0.57), and positively correlated with systemic vascular resistance (r= +0.57), as well as thoracic fluid content (r= +0.43). QRS duration alone was not specifically associated with any hemodynamic parameter, but JTc interval positively correlated with total arterial compliance (r=+0.42). Conclusions: In heart failure patients, we interestingly found that increased systemic vascular resistance results in QTc interval prolongation, where repolarization time is specifically influenced by arterial compliance. This suggests potential benefit from antihypertensive therapy targeted at lowering systemic vascular resistance in those with prolonged QTc/JTc. Nevertheless, these intervals need to be interpreted with caution in patients with thoracic fluid overload (e.g., pulmonary edema).

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Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.1.h126 ◽

1987 ◽

Vol 253 (1) ◽

pp. H126-H132

Author(s):

R. W. Lee ◽

L. D. Lancaster ◽

D. Buckley ◽

S. Goldman

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Systemic Vascular Resistance ◽

Vascular Resistance ◽

Arterial Compliance ◽

Peripheral Circulation ◽

Aortic Pressure ◽

Venous Compliance ◽

Mean Aortic Pressure

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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