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Hemodynamic Significance (hemodynamic + significance)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Usefulness of translesional pressure gradient and pharmacological provocation for the assessment of intermediate renal artery disease

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 3 2006
Noah J. Jones MD
Abstract Objective: We sought to determine the hemodynamic significance of intermediate RAS by measuring translesional systolic pressure gradients (TSPG), using a pressure-sensing guidewire at baseline and after acetylcholine (ACh) induced hyperemia, following selective renal artery angiography. Background: Renal artery stenosis (RAS) is a cause of reversible hypertension and nephropathy. Stenting effectively relieves RAS, however improvement in blood pressure control or renal function is variable and unpredictable. Hemodynamic significance is usually present with RAS when diameter stenosis is >75%, but is less predictable in intermediate (30%,75%) RAS. Methods: Twenty-two patients (26 renal arteries) with uncontrolled hypertension underwent invasive hemodynamic assessment because of intermediate RAS, defined as radiocontrast angiographic diameter stenosis (DS) between 30% and 75% (quantitative DS was measured prospectively). Translesional pressure gradients were measured using a 0.014" pressure-sensing wire. Hyperemia was induced by administration of intrarenal ACh. Results: Visual and measured angiographic lesion severity did not correlate with TSPG either at baseline (visual DS, R2 = 0.091, P = 0.13; measured DS, R2 = 0.124, P = 0.07) or with hyperemia (visual DS, R2 = 0.057, P = 0.24; measured DS, R2 = 0.101, P = 0.12). Baseline and maximal hyperemic gradient did correlate (R2 = 0.567; P < 0.05). Pharmacological provocation produced a significant increase in TSPG (mean; baseline, 18 ± 21 vs. hyperemia, 34 ± 41 mm Hg; P < 0.05). A hemodynamically significant lesion (TSPG > 20 mm Hg) was found in 14/26 (54%) arteries (13 patients); 13 (60%) patients subsequently underwent renal artery stenting for hemodynamically significant RAS. At follow-up (at least 30 days), there was a significant decrease in systolic blood pressure (mean; 167 ± 24 vs. 134 ± 19 mm Hg; P < 0.001). Conclusions: Intrarenal administration of ACh induces hyperemia and can be used to unmask resistive renal artery lesions. Gradient measurement and induced hyperemia may be warranted in the invasive assessment of intermediate renal artery stenoses, rather than relying on stenosis severity alone. Further study is needed to determine whether translesional pressure gradients and pharmacological provocation predict clinical benefit after renal artery stenting. © 2006 Wiley-Liss, Inc. [source]

Hemodynamic significance of heart rate in neurally mediated syncope

CLINICAL CARDIOLOGY, Issue 11 2004
Wan Leong Chan M.D.
Abstract Background: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. Methods: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). Results: The baseline hemodynamic data (mean ± standard deviation) and the hemodynamic responses after 10-min head-up tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 ± 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 ± 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 ±0.29 vs. 1.97 ±0.41 l/min/m2, p< 0.001 and 2098 ± 615 vs. 1573 ± 353 dynes·s·cm,5·m2, p<0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. Conclusions: These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope. [source]

Coronary pressure never lies

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2008
Jacques J. Koolen MD
Abstract Fractional Flow Reserve (FFR), calculated by coronary pressure measurement, is the invasive gold standard to assess the hemodynamic significance of a coronary stenosis. FFR reliably indicates whether a stenosis is responsible for inducible ischemia and if percutaneous coronary intervention is appropriate. False positive or negative FFR is rare. Occasionally, however, a clinical or angiographic condition is encountered in which in first instance the FFR measurement contradicts the intuitive feeling of the interventionalist. Further examination in such cases, however, often reveals a clear physiologic explanation and in this manner FFR "lifts the veil". Two such patients are presented in this case report and the reasons for apparent or actual false positive or negative FFR are discussed. © 2008 Wiley-Liss, Inc. [source]

Usefulness of translesional pressure gradient and pharmacological provocation for the assessment of intermediate renal artery disease

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 3 2006
Noah J. Jones MD
Abstract Objective: We sought to determine the hemodynamic significance of intermediate RAS by measuring translesional systolic pressure gradients (TSPG), using a pressure-sensing guidewire at baseline and after acetylcholine (ACh) induced hyperemia, following selective renal artery angiography. Background: Renal artery stenosis (RAS) is a cause of reversible hypertension and nephropathy. Stenting effectively relieves RAS, however improvement in blood pressure control or renal function is variable and unpredictable. Hemodynamic significance is usually present with RAS when diameter stenosis is >75%, but is less predictable in intermediate (30%,75%) RAS. Methods: Twenty-two patients (26 renal arteries) with uncontrolled hypertension underwent invasive hemodynamic assessment because of intermediate RAS, defined as radiocontrast angiographic diameter stenosis (DS) between 30% and 75% (quantitative DS was measured prospectively). Translesional pressure gradients were measured using a 0.014" pressure-sensing wire. Hyperemia was induced by administration of intrarenal ACh. Results: Visual and measured angiographic lesion severity did not correlate with TSPG either at baseline (visual DS, R2 = 0.091, P = 0.13; measured DS, R2 = 0.124, P = 0.07) or with hyperemia (visual DS, R2 = 0.057, P = 0.24; measured DS, R2 = 0.101, P = 0.12). Baseline and maximal hyperemic gradient did correlate (R2 = 0.567; P < 0.05). Pharmacological provocation produced a significant increase in TSPG (mean; baseline, 18 ± 21 vs. hyperemia, 34 ± 41 mm Hg; P < 0.05). A hemodynamically significant lesion (TSPG > 20 mm Hg) was found in 14/26 (54%) arteries (13 patients); 13 (60%) patients subsequently underwent renal artery stenting for hemodynamically significant RAS. At follow-up (at least 30 days), there was a significant decrease in systolic blood pressure (mean; 167 ± 24 vs. 134 ± 19 mm Hg; P < 0.001). Conclusions: Intrarenal administration of ACh induces hyperemia and can be used to unmask resistive renal artery lesions. Gradient measurement and induced hyperemia may be warranted in the invasive assessment of intermediate renal artery stenoses, rather than relying on stenosis severity alone. Further study is needed to determine whether translesional pressure gradients and pharmacological provocation predict clinical benefit after renal artery stenting. © 2006 Wiley-Liss, Inc. [source]

Hemodynamic significance of heart rate in neurally mediated syncope

CLINICAL CARDIOLOGY, Issue 11 2004
Wan Leong Chan M.D.
Abstract Background: Vasovagal and vasodepressor syncope are used interchangeably in the literature to describe the common faint syndrome, now collectively named neurally mediated syncope. The significance of heart rate (HR) in these reflex-induced reactions remains unclear. Hypothesis: The study was undertaken to investigate the hemodynamic significance of HR in tilt-induced neurally mediated syncope. Methods: In all, 113 patients with syncope of unknown etiology were studied by head-up tilt test with invasive hemodynamic monitoring. Thirty-five patients (15 women, 20 men, age range 21 to 72 years) developed syncope and were enrolled for analysis. The hemodynamic data were compared between patients who developed bradycardia (vasovagal group, n = 15) and those without bradycardia (vasodepressor group, n = 20). Results: The baseline hemodynamic data (mean ± standard deviation) and the hemodynamic responses after 10-min head-up tilt were similar between patients in the vasovagal and vasodepressor groups. During syncope, patients with vasovagal reaction developed hypotension and paradoxical bradycardia (HR = 52.4 ± 5.9 beats/min), while patients with vasodepressor reaction developed a precipitous drop in arterial blood pressure with inappropriate HR (105 ± 21 beats/min) compensation. Patients with vasovagal syncope manifested a significantly lower cardiac index and a significantly higher systemic vascular resistance index than patients with vasodepressor syncope (1.47 ±0.29 vs. 1.97 ±0.41 l/min/m2, p< 0.001 and 2098 ± 615 vs. 1573 ± 353 dynes·s·cm,5·m2, p<0.003, respectively). A positive correlation existed between HR and cardiac index (r = 0.44, p = 0.008) during syncope in the patients studied. Conclusions: These findings suggest that the hemodynamic characteristics of vasovagal and vasodepressor reactions are different, and that HR plays a significant role in neurally mediated syncope. [source]