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Jan J Piek - One of the best experts on this subject based on the ideXlab platform.
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contribution of age related microvascular dysfunction to abnormal Coronary Hemodynamics in patients with ischemic heart disease
Jacc-cardiovascular Interventions, 2020Co-Authors: Tim P Van De Hoef, Mauro Echavarriapinto, Javier Escaned, Martijn Meuwissen, Valerie E Stegehuis, Jan J PiekAbstract:Abstract Objectives This study sought to investigate the contribution of age-related microcirculatory dysfunction to abnormal Coronary Hemodynamics in patients with Coronary atherosclerosis. Background Impairment in myocardial blood supply in patients with Coronary atherosclerosis can be accentuated due to age-related changes in microcirculatory function. Methods IntraCoronary pressure and flow were measured with the Doppler technique in 299 vessels (228 patients), and the thermodilution technique in 120 vessels (99 patients). In 172 patients, Doppler measurements were also performed in unobstructed vessels. Associations of Coronary Hemodynamics with aging were studied in both the stenosed and unobstructed arteries. Results Aging was associated with a progressive increase in minimal microvascular resistance and a progressive decrease in hyperemic flow in both obstructed and nonobstructed Coronary arteries. As such, Coronary flow reserve decreased with advancing age. Epicardial stenosis severity assessed by resting Pd/Pa, basal stenosis resistance index, and hyperemic stenosis resistance index was equivalent across age groups. By contrast, fractional flow reserve increased with advancing age. Consequently, the adjusted risk of a fractional flow reserve/Coronary flow reserve pattern reflective of concomitant focal epicardial and diffuse or microvascular disease (relative risk: 1.6; 95% confidence interval: 1.1 to 2.3; p = 0.017) increased with advancing age, whilst the adjusted risk of a fractional flow reserve/Coronary flow reserve pattern reflective of non–flow-limiting stenosis with a healthy microcirculation decreased (relative risk: 0.7; 95% CI: 0.5 to 1.0; p = 0.022). Conclusions Aging is associated with progressive pan-myocardial impairment of Coronary vasodilatory capacity due to an increase in minimal microvascular resistance. Concomitant aging-related impairment in microvascular function impacts the pathophysiology of ischemic heart disease in the individual patient and is not adequately identified by hyperemic Coronary pressure measurements alone.
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impact of aortic valve stenosis on Coronary Hemodynamics and the instantaneous effect of transcatheter aortic valve implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Cristina M Rolandi, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P <0.001). Improvement in Coronary Hemodynamics after TAVI was most pronounced in patients without post-TAVI aortic regurgitation. In these patients (n=20), hyperemic flow velocity increased significantly from 46.24±15.47 pre-TAVI to 56.56±17.44 cm/s post-TAVI ( P =0.003). Hyperemic microvascular resistance decreased from 2.03±0.71 to 1.66±0.45 ( P =0.050). Coronary flow velocity reserve increased significantly from 1.9±0.4 to 2.2±0.6 ( P =0.009). Conclusions— The vasodilatory reserve capacity of the Coronary circulation is reduced in AS. TAVI induces an immediate decrease in hyperemic microvascular resistance and a concomitant increase in hyperemic flow velocity, resulting in immediate improvement in Coronary vasodilatory reserve.
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Impact of Aortic Valve Stenosis on Coronary Hemodynamics and the Instantaneous Effect of Transcatheter Aortic Valve Implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, M. Cristina Rolandi, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P
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effects of left ventricular unloading by impella recover lp2 5 on Coronary Hemodynamics
Catheterization and Cardiovascular Interventions, 2007Co-Authors: Maurice Remmelink, Karel T Koch, Jan J Piek, Krischan D Sjauw, Jose P S Henriques, Robbert J De Winter, Rene J Van Der Schaaf, Jan G P Tijssen, Jan BaanAbstract:Objectives: We studied the effects of LV unloading by the Impella on Coronary Hemodynamics by simultaneously measuring intraCoronary pressure and flow and the derived parameters fractional flow reserve (FFR), Coronary flow velocity reserve (CFVR), and Coronary microvascular resistance (MR). Background: Patients with compromised left ventricular (LV) function undergoing high-risk percutaneous Coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on Coronary Hemodynamics. Methods: Eleven patients (mean LV ejection fraction of 35 ± 11%) underwent PCI during LV support by the LV unloading device (Impella Recover® LP2.5). IntraCoronary measurements were performed in a nonstenotic Coronary artery after the PCI, before and after adenosine-induced hyperemia at four different support levels (0–2.5 L/min). Results: Aortic and Coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 ± 24 to 72 ± 27 cm/sec, P = 0.001 and 1.88 ± 0.52 to 2.34 ± 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 ± 1.32 to 1.89 ± 1.43 mm Hg cm−1 sec, P = 0.005). Conclusions: Unloading of the LV by the Impella increased aortic and intraCoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella-induced increase in Coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance. © 2007 Wiley-Liss, Inc.
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Coronary Hemodynamics of stent implantation after suboptimal and optimal balloon angioplasty
Journal of the American College of Cardiology, 2002Co-Authors: Michiel Voskuil, Jan G P Tijssen, Rob A M Van Liebergen, Mariano Albertal, Eric Boersma, Patrick W Serruys, Jan J PiekAbstract:Abstract Objectives This study was performed to evaluate hemodynamic alterations of stent implantation after Doppler flow–guided balloon angioplasty (BA). Background There is controversy regarding the effect of stent implantation on Coronary Hemodynamics after suboptimal and optimal BA. Methods A total of 523 of 620 patients underwent Doppler-guided BA in the setting of a multicenter study and were analyzed before and after additional stent implantation. Balloon angioplasty was considered optimal when the diameter stenosis (DS) was ≤35% and Coronary flow reserve (CFR) was >2.5 and suboptimal if these two criteria were not met. Coronary flow reserve was also measured in an angiographically normal artery to determine relative CFR. Patients were followed for 12 months to document major adverse cardiac events (MACE). Results The main difference between patients with suboptimal BA (n = 195 [51%]) and optimal BA (n = 184 [49%]) was a more pronounced increase in baseline blood flow velocity (15 ± 8 to 22 ± 11 vs. 14 ± 8 to 16 ± 10 cm/s, p Conclusions Stent implantation enhances CFR after suboptimal and optimal Doppler-guided BA, owing to a reduction in residual lumen obstruction—determined by angiographical and Doppler flow criteria—as the underlying mechanism for an improved clinical outcome.
Jan Baan - One of the best experts on this subject based on the ideXlab platform.
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impact of aortic valve stenosis on Coronary Hemodynamics and the instantaneous effect of transcatheter aortic valve implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Cristina M Rolandi, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P <0.001). Improvement in Coronary Hemodynamics after TAVI was most pronounced in patients without post-TAVI aortic regurgitation. In these patients (n=20), hyperemic flow velocity increased significantly from 46.24±15.47 pre-TAVI to 56.56±17.44 cm/s post-TAVI ( P =0.003). Hyperemic microvascular resistance decreased from 2.03±0.71 to 1.66±0.45 ( P =0.050). Coronary flow velocity reserve increased significantly from 1.9±0.4 to 2.2±0.6 ( P =0.009). Conclusions— The vasodilatory reserve capacity of the Coronary circulation is reduced in AS. TAVI induces an immediate decrease in hyperemic microvascular resistance and a concomitant increase in hyperemic flow velocity, resulting in immediate improvement in Coronary vasodilatory reserve.
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Impact of Aortic Valve Stenosis on Coronary Hemodynamics and the Instantaneous Effect of Transcatheter Aortic Valve Implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, M. Cristina Rolandi, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P
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effects of left ventricular unloading by impella recover lp2 5 on Coronary Hemodynamics
Catheterization and Cardiovascular Interventions, 2007Co-Authors: Maurice Remmelink, Karel T Koch, Jan J Piek, Krischan D Sjauw, Jose P S Henriques, Robbert J De Winter, Rene J Van Der Schaaf, Jan G P Tijssen, Jan BaanAbstract:Objectives: We studied the effects of LV unloading by the Impella on Coronary Hemodynamics by simultaneously measuring intraCoronary pressure and flow and the derived parameters fractional flow reserve (FFR), Coronary flow velocity reserve (CFVR), and Coronary microvascular resistance (MR). Background: Patients with compromised left ventricular (LV) function undergoing high-risk percutaneous Coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on Coronary Hemodynamics. Methods: Eleven patients (mean LV ejection fraction of 35 ± 11%) underwent PCI during LV support by the LV unloading device (Impella Recover® LP2.5). IntraCoronary measurements were performed in a nonstenotic Coronary artery after the PCI, before and after adenosine-induced hyperemia at four different support levels (0–2.5 L/min). Results: Aortic and Coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 ± 24 to 72 ± 27 cm/sec, P = 0.001 and 1.88 ± 0.52 to 2.34 ± 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 ± 1.32 to 1.89 ± 1.43 mm Hg cm−1 sec, P = 0.005). Conclusions: Unloading of the LV by the Impella increased aortic and intraCoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella-induced increase in Coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance. © 2007 Wiley-Liss, Inc.
Kanu Chatterjee - One of the best experts on this subject based on the ideXlab platform.
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Review Article Coronary Hemodynamics in Heart Failure and Effects of Therapeutic Interventions
2020Co-Authors: Kanu ChatterjeeAbstract:Background: The abnormalities in Coronary Hemodynamics in systolic heart failure are frequent. Myocardial oxygen demand and consumption are increased and myocardial perfusion is also impaired, which may result in myocardial ischemia, necrosis, and apoptosis. This is potentially a contributing factor for progressive heart failure. Methods and Results: Neurohormonal abnormalities such as activated renin-angiotensin-aldosterone system, increased adrenergic activity, hemodynamic abnormalities such as decreased left ventricular perfusion pressure,andincreasedleftventriculardiastolicpressureareimportantmechanismsformyocardialischemia. Conclusions: Different pharmacologic agents may exert different effects on Coronary Hemodynamics although changes in systemic Hemodynamics may be similar. Some agents may enhance myocardial ischemia and others may decrease it. Thus, an understanding of changes in Coronary Hemodynamics may have therapeutic implications. (J Cardiac Fail 2009;15:116e123) Abnormalities in Coronary Hemodynamics in systolic heart failure are frequent and may be contributing mechanisms in ventricular remodeling, myocardialdysfunction, and progressive heart failure. Furthermore, potential beneficial or adverse effects on Coronary Hemodynamics during therapeutic interventions are frequently ignored, but the changes in Coronary Hemodynamics during such treatments have therapeutic and prognostic implications. In this review, the changes in Coronary Hemodynamics and the effects of commonly used therapies for systolic heart failure will be discussed.
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Coronary Hemodynamics in heart failure and effects of therapeutic interventions
Journal of Cardiac Failure, 2009Co-Authors: Kanu ChatterjeeAbstract:BACKGROUND: The abnormalities in Coronary Hemodynamics in systolic heart failure are frequent. Myocardial oxygen demand and consumption are increased and myocardial perfusion is also impaired, which may result in myocardial ischemia, necrosis, and apoptosis. This is potentially a contributing factor for progressive heart failure. METHODS AND RESULTS: Neurohormonal abnormalities such as activated renin-angiotensin-aldosterone system, increased adrenergic activity, hemodynamic abnormalities such as decreased left ventricular perfusion pressure, and increased left ventricular diastolic pressure are important mechanisms for myocardial ischemia. CONCLUSIONS: Different pharmacologic agents may exert different effects on Coronary Hemodynamics although changes in systemic Hemodynamics may be similar. Some agents may enhance myocardial ischemia and others may decrease it. Thus, an understanding of changes in Coronary Hemodynamics may have therapeutic implications.
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Flosequinan, a new vasodilator: systemic and Coronary Hemodynamics and neuroendocrine effects in congestive heart failure.
Journal of the American College of Cardiology, 1992Co-Authors: Patricia G. Cavero, Teresa De Marco, Michael Kwasman, Kanu ChatterjeeAbstract:Objectives. The aim of this study was to evaluate the immediate and long-term systemic and Coronary hemodynamic, metabolic and neurohormonal effects of flosequinan in patients with congestive heart failure. Background. Preliminary studies have shown that this new long-acting oral systemic vasodilator may have beneficial effects in patients with heart failure. Methods. Thirteen patients with congestive heart failure were studied. Systemic and Coronary hemodynamic, metabolic and neurohormonal effects of flosequinan were assessed acutely with repeat systemic hemodynamic studies after 6 weeks of treatment. Results. The administration of flosequinan acutely and after long-term treatment, resulted in a significant increase in cardiac index, stroke work index and stroke volume index with a reduction in systemic and pulmonary vascular resistances. The improvement in ventricular function was associated with an improvement in left ventricular efficiency without a change in myocardial oxygen consumption or Coronary sinus blood flow. Myocardial oxygen extraction and net myocardial lactate extraction also did not change significantly with flosequinan therapy. Systemic catecholamine levels and myocardial catecholamine balance did not change. Plasma arterial and Coronary sinus atrial natriuretic factor concentrations were elevated at baseline; the latter concentrations at the level of the great cardiac vein were significantly higher than those of arterial concentrations, indicating increased left ventricular release of atrial natriuretic factor in congestive heart failure. Both arterial and Coronary sinus atrial natriuretic factor levels were significantly reduced with the administration of flosequinan at peak effect in association with an improvement in systemic Hemodynamics. Conclusions. Flosequinan therapy in patients with congestive heart failure results in a sustained beneficial hemodynamic action and improved cardiac performance without an increase in metabolic demand or activation of the sympathetic nervous system.
Tim P Van De Hoef - One of the best experts on this subject based on the ideXlab platform.
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contribution of age related microvascular dysfunction to abnormal Coronary Hemodynamics in patients with ischemic heart disease
Jacc-cardiovascular Interventions, 2020Co-Authors: Tim P Van De Hoef, Mauro Echavarriapinto, Javier Escaned, Martijn Meuwissen, Valerie E Stegehuis, Jan J PiekAbstract:Abstract Objectives This study sought to investigate the contribution of age-related microcirculatory dysfunction to abnormal Coronary Hemodynamics in patients with Coronary atherosclerosis. Background Impairment in myocardial blood supply in patients with Coronary atherosclerosis can be accentuated due to age-related changes in microcirculatory function. Methods IntraCoronary pressure and flow were measured with the Doppler technique in 299 vessels (228 patients), and the thermodilution technique in 120 vessels (99 patients). In 172 patients, Doppler measurements were also performed in unobstructed vessels. Associations of Coronary Hemodynamics with aging were studied in both the stenosed and unobstructed arteries. Results Aging was associated with a progressive increase in minimal microvascular resistance and a progressive decrease in hyperemic flow in both obstructed and nonobstructed Coronary arteries. As such, Coronary flow reserve decreased with advancing age. Epicardial stenosis severity assessed by resting Pd/Pa, basal stenosis resistance index, and hyperemic stenosis resistance index was equivalent across age groups. By contrast, fractional flow reserve increased with advancing age. Consequently, the adjusted risk of a fractional flow reserve/Coronary flow reserve pattern reflective of concomitant focal epicardial and diffuse or microvascular disease (relative risk: 1.6; 95% confidence interval: 1.1 to 2.3; p = 0.017) increased with advancing age, whilst the adjusted risk of a fractional flow reserve/Coronary flow reserve pattern reflective of non–flow-limiting stenosis with a healthy microcirculation decreased (relative risk: 0.7; 95% CI: 0.5 to 1.0; p = 0.022). Conclusions Aging is associated with progressive pan-myocardial impairment of Coronary vasodilatory capacity due to an increase in minimal microvascular resistance. Concomitant aging-related impairment in microvascular function impacts the pathophysiology of ischemic heart disease in the individual patient and is not adequately identified by hyperemic Coronary pressure measurements alone.
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impact of aortic valve stenosis on Coronary Hemodynamics and the instantaneous effect of transcatheter aortic valve implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Cristina M Rolandi, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P <0.001). Improvement in Coronary Hemodynamics after TAVI was most pronounced in patients without post-TAVI aortic regurgitation. In these patients (n=20), hyperemic flow velocity increased significantly from 46.24±15.47 pre-TAVI to 56.56±17.44 cm/s post-TAVI ( P =0.003). Hyperemic microvascular resistance decreased from 2.03±0.71 to 1.66±0.45 ( P =0.050). Coronary flow velocity reserve increased significantly from 1.9±0.4 to 2.2±0.6 ( P =0.009). Conclusions— The vasodilatory reserve capacity of the Coronary circulation is reduced in AS. TAVI induces an immediate decrease in hyperemic microvascular resistance and a concomitant increase in hyperemic flow velocity, resulting in immediate improvement in Coronary vasodilatory reserve.
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Impact of Aortic Valve Stenosis on Coronary Hemodynamics and the Instantaneous Effect of Transcatheter Aortic Valve Implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, M. Cristina Rolandi, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P
Karel T Koch - One of the best experts on this subject based on the ideXlab platform.
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impact of aortic valve stenosis on Coronary Hemodynamics and the instantaneous effect of transcatheter aortic valve implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Cristina M Rolandi, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P <0.001). Improvement in Coronary Hemodynamics after TAVI was most pronounced in patients without post-TAVI aortic regurgitation. In these patients (n=20), hyperemic flow velocity increased significantly from 46.24±15.47 pre-TAVI to 56.56±17.44 cm/s post-TAVI ( P =0.003). Hyperemic microvascular resistance decreased from 2.03±0.71 to 1.66±0.45 ( P =0.050). Coronary flow velocity reserve increased significantly from 1.9±0.4 to 2.2±0.6 ( P =0.009). Conclusions— The vasodilatory reserve capacity of the Coronary circulation is reduced in AS. TAVI induces an immediate decrease in hyperemic microvascular resistance and a concomitant increase in hyperemic flow velocity, resulting in immediate improvement in Coronary vasodilatory reserve.
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Impact of Aortic Valve Stenosis on Coronary Hemodynamics and the Instantaneous Effect of Transcatheter Aortic Valve Implantation
Circulation-cardiovascular Interventions, 2015Co-Authors: Esther M A Wiegerinck, Tim P Van De Hoef, Zeyie Yong, Floortje Van Kesteren, Karel T Koch, Jan J Piek, M. Cristina Rolandi, Jan BaanAbstract:Background— Aortic valve stenosis (AS) induces compensatory alterations in left ventricular Hemodynamics, leading to physiological and pathological alterations in Coronary Hemodynamics. Relief of AS by transcatheter aortic valve implantation (TAVI) decreases ventricular afterload and is expected to improve microvascular function immediately. We evaluated the effect of AS on Coronary Hemodynamics and the immediate effect of TAVI. Methods and Results— IntraCoronary pressure and flow velocity were simultaneously assessed at rest and at maximal hyperemia in an unobstructed Coronary artery in 27 patients with AS before and immediately after TAVI and in 28 patients without AS. Baseline flow velocity was higher and baseline microvascular resistance was lower in patients with AS as compared with controls, which remained unaltered post-TAVI. In patients with AS, hyperemic flow velocity was significantly lower as compared with controls (44.5±14.5 versus 54.3±18.6 cm/s; P =0.04). Hyperemic microvascular resistance (expressed in mm Hg·cm·s−1) was 2.10±0.69 in patients with AS as compared with 1.80±0.60 in controls ( P =0.096). Coronary flow velocity reserve in patients with AS was lower, 1.9±0.5 versus 2.7±0.7 in controls ( P
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effects of left ventricular unloading by impella recover lp2 5 on Coronary Hemodynamics
Catheterization and Cardiovascular Interventions, 2007Co-Authors: Maurice Remmelink, Karel T Koch, Jan J Piek, Krischan D Sjauw, Jose P S Henriques, Robbert J De Winter, Rene J Van Der Schaaf, Jan G P Tijssen, Jan BaanAbstract:Objectives: We studied the effects of LV unloading by the Impella on Coronary Hemodynamics by simultaneously measuring intraCoronary pressure and flow and the derived parameters fractional flow reserve (FFR), Coronary flow velocity reserve (CFVR), and Coronary microvascular resistance (MR). Background: Patients with compromised left ventricular (LV) function undergoing high-risk percutaneous Coronary intervention (PCI) may benefit from LV unloading. Limited information is available on the effects of LV unloading on Coronary Hemodynamics. Methods: Eleven patients (mean LV ejection fraction of 35 ± 11%) underwent PCI during LV support by the LV unloading device (Impella Recover® LP2.5). IntraCoronary measurements were performed in a nonstenotic Coronary artery after the PCI, before and after adenosine-induced hyperemia at four different support levels (0–2.5 L/min). Results: Aortic and Coronary pressure increased with increasing support levels, whereas FFR remained unchanged. Baseline flow velocity remained unchanged, while hyperemic flow velocity and CFVR increased significantly with increasing support levels (61 ± 24 to 72 ± 27 cm/sec, P = 0.001 and 1.88 ± 0.52 to 2.34 ± 0.63, P < 0.001 respectively). The difference between baseline MR and hyperemic MR significantly increased with increasing support levels (1.28 ± 1.32 to 1.89 ± 1.43 mm Hg cm−1 sec, P = 0.005). Conclusions: Unloading of the LV by the Impella increased aortic and intraCoronary pressure, hyperemic flow velocity and CFVR, and decreased MR. The Impella-induced increase in Coronary flow, probably results from both an increased perfusion pressure and a decreased LV volume-related intramyocardial resistance. © 2007 Wiley-Liss, Inc.