Average Peak Flow Velocity Research Articles

Decreasing the blood flow of non-compressible intra-abdominal organs with non-invasive transcutaneous electrical stimulation

Non-invasive neuromodulation of non-compressible internal organs has significant potential for internal organ bleeding and blood-shift in aero/space medicine. The present study aims to investigate the potential influences of the non-invasive transcutaneous electrical nerve stimulation (TENS) on multiple non-compressible internal organs’ blood flow. Porcine animal model (n = 8) was randomized for a total of 48 neuromodulation sessions with two different TENS stimulation frequencies (80 Hz, 10 Hz) and a placebo stimulation. A combination of two different electrode configurations (Abdominal-only or Abdominal and hind limb) were also performed. Intraarterial blood flow measurements were taken during pre and post-stimulation periods at the left renal artery, common hepatic artery, and left coronary artery. Intracranial, and extracranial arterial blood flows were also assessed with digital subtraction angiography. TENS with abdominal-only electrode configurations at 10 Hz demonstrated significant reductions in average peak blood flow velocity (APV) of the common hepatic artery (p = 0.0233) and renal arteries (p = 0.0493). Arterial pressures (p = 0.0221) were also significantly lower when renal APV was reduced. The outcome of the present study emphasises the potential use of TENS in decreasing the blood flow of non-compressible internal organs when the correct combination of electrodes configuration and frequency is used.

Abstract 10045: Higher Renal Vascular Resistance is Associated With Greater Body Mass Index in Children

Background: Obesity is associated with increased risk for cardiovascular and renal diseases, however, there has been little focus on renal vascular function. The purpose of this study is to assess renal vascular flow regulation and investigate their relation to cardiovascular risk factors in obese children. Methods: Noninvasive ultrasonographic measurements were made in 108 overweight/obese children aged 7 to 13 years (body mass index 18 to 33kg/m 2 ). Using color Doppler sonography, peak systolic (PSV), end-diastolic (EDV), and average peak flow (APV) velocities of renal artery were measured. Pulsatility index as a parameter of vascular resistance was calculated. Pulsatility index was defined as (PSV-EDV)/APV. Quantitative B-mode ultrasound scans were used to measure intima-media thickness and diameters of the common carotid artery. Plasma lipid concentrations, uric acid, homeostasis model assessment of insulin resistance, and high sensitivity C-reactive protein were assessed in the obese children. Results: Compared with overweight children with body mass index <25 kg/m 2 , pulsatility index in obese children with body mass index≥25 kg/m 2 was significantly higher (1.24 ±0.13 vs. 1.13 ±0.14 cm/sec, p < 0.01), because APV and EDV were significantly lower (35 ±3 vs. 38 ±7 cm/sec and 21± 3 vs. 25 ±5 cm/sec, p <0.05, respectively), although PSV was not significantly different. Pulsatility index correlated significantly with body mass index (r =0.58, p < 0.01), insulin (r = 0.24, p < 0.05), homeostasis model assessment of insulin resistance (r =0.25, p < 0.01), triglycerides (r = 0.26, p < 0.01), uric acid (r = 0.22, p < 0.05), systolic blood pressure (r = 0.31, p < 0.01), and carotid intima-media thickness (r = 0.36, p<0.01). Renal blood flow velocities did not correlate with high sensitivity C-reactive protein. Conclusions: The present study indicates that obesity can adversely affect renal vascular flow and resistance in children. Obesity-related insulin resistance may be a main risk factor for renal vascular flow changes. Obesity not only is a risk factor for later cardiovascular disease, but also is associated with significant impairment of renal arterial flow dynamics.

Differential impact of coronary revascularization on long-term clinical outcome according to coronary flow characteristics: analysis of the international ILIAS registry

Abstract Backgrounds Coronary pressure indices such as fractional flow reserve (FFR) are standard in guiding elective revascularization. However, considering additional coronary flow parameters could further individualize and optimize the decision on revascularization, especially in terms of the impact on prognosis. We aimed to investigate the potentially differential prognostic associations of elective PCI according to coronary flow properties represented by coronary flow reserve (CFR), coronary flow capacity (CFC) and baseline CFC (bCFC). Methods From the Inclusive invasive physiological assessment in angina syndromes (ILIAS) registry composed of 16 hospitals globally from 7 countries, patients with obstructive coronary artery disease who underwent invasive coronary physiological assessment were included (N=2370 vessels). We assessed effect measure modifications of the association of PCI and 5-year target vessel failure (TVF) according to CFR, CFC and bCFC either assessed by Doppler-technique or thermodilution-method in three models: conditional logistic regression, marginal structural model, and COX proportional hazard model. Reduced CFR, CFC and bCFC were defined as CFR<2.1, CFR<2.1 with hyperemic average peak flow velocity (APV)<33.8 cm/s, and CFR<2.1 with baseline APV>17.0 cm/s in Doppler-technique, respectively (Figure 1), and the corresponding percentiles in thermodilution-methods. All models were adjusted for FFR, the interaction between PCI and FFR, and other confounders. Results The mean age of the population was 63.3 years and there were 1322 (73.6%) males. Median FFR was 0.85 and PCI was performed in 600 (25.3%) vessels. Reduced CFR, CFC, and abnormal bCFC were defined in 988 (41.7%), 542 (22.9%), and 600 (25.3%) vessels, respectively. There were little overlaps in vessels with reduced CFC and abnormal bCFC. In univariate analyses, vessels with reduced CFC had worse outcomes compared with those with normal CFC if deferred (13.4% vs. 6.6%), whereas reduced CFC was associated with better prognosis if treated by PCI (9.5% vs. 11.3%). Significant effect measure modifications were observed by CFC either in odds ratio (P=0.0018), additive (P=0.029), and hazard ratio scale (P=0.0002) (Figure 2). Vessels with reduced CFC had, compared with those with normal CFC, higher adjusted absolute risk of 5-year TVF by 5.9 [0.1, 12] percent if deferred, but lower risk by 1.8 [−1.7, 5.3] percent if treated by PCI. CFR and bCFC were not significant effect modifiers in any scales. Similar associations were observed in per-patient analyses, whereas the findings were less robust. Conclusions We observed a beneficial impact of PCI on absolute risk of 5-year clinical outcomes in vessels with reduced CFC, and a detrimental effect in those with normal CFC. CFR and bCFC were not robust effect modifiers of PCI. Therefore, CFC, combined with FFR, could be potentially used to optimize the patient selection for elective PCI treatment. Funding Acknowledgement Type of funding sources: None.

Comparison of fractional flow reserve, instantaneous wave-free ratio and a novel technique for assessing coronary arteries with serial lesions.

Physiological indices such as fractional flow reserve (FFR), instantaneous wave-free ratio (iFR) and resting distal coronary to aortic pressure (Pd/Pa) are increasingly used to guide revascularisation. However, reliable assessment of individual stenoses in serial coronary disease remains an unmet need. This study aimed to compare conventional pressure-based indices, a reference Doppler-based resistance index (hyperaemic stenosis resistance [hSR]) and a recently described mathematical correction model to predict the contribution of individual stenoses in serial disease. Resting and hyperaemic pressure wire pullbacks were performed in 54 patients with serial disease. For each stenosis, FFR, iFR, and Pd/Pa were measured by the translesional gradient in each index and the predicted FFR (FFRpred) derived mathematically from hyperaemic pullback data. "True" stenosis significance by each index was assessed following PCI of the accompanying stenosis or measurements made in a large disease-free branch. In 27 patients, Doppler average peak flow velocity (APV) was also measured to calculate hSR (hSR=∆P/APV, where ∆P=translesional pressure gradient). FFR underestimated individual stenosis severity, inversely proportional to cumulative FFR (r=0.5, p<0.001). Mean errors for FFR, iFR and Pd/Pa were 33%, 20% and 24%, respectively, and 14% for FFRpred (p<0.001). Stenosis misclassification rates based on FFR 0.80, iFR 0.89 and Pd/Pa 0.91 thresholds were not significantly different (17%, 24% and 20%, respectively) but were higher than FFRpred (11%, p<0.001). Apparent and true hSR correlated strongly (r=0.87, p<0.001, mean error 0.19±0.3), with only 7% of stenoses misclassified. Individual stenosis severity is significantly underestimated in the presence of serial disease, using both hyperaemic and resting pressure-based indices. hSR is less prone to error but challenges in optimising Doppler signals limit clinical utility. A mathematical correction model, using data from hyperaemic pressure wire pullback, produces similar accuracy to hSR and is superior to conventional pressure-based indices.

The Monitoring and Application of Transcranial Doppler Ultrasound in Patients with Severe Neurovascular Diseases

To investigate the monitoring effect and application of transcranial Doppler ultrasound (TCD) in patients with severe neurovascular cerebrovascular diseases. From December 2016 to October 2018, 96 patients with cerebrovascular disease in Department of Neurology and ICU, West China Hospital, Sichuan University were monitored by bedside TCD, including the detection of bilateral middle cerebral arteries (MCAs) through temporal window, and the detection of the basilar artery (BA) through occipital window, characterized by the peak systolic blood flow velocity, peak diastolic blood flow velocity, average peak blood flow velocity, vascular pulsatility index, vascular pulsatility index, vascular resistance index and blood flow spectrum morphology in local hemodynamic changes. According to the monitoring results, it was divided into vasospasm group, increased blood flow group and insufficient blood supply group. Relevant data of monitoring results were analysed. Bedside TCD monitoring was successfully used to all cerebrovascular diseases patients. Among 96 patients, 37 patients (38.54%) had increased cerebral blood flow, 15 patients (15.62%) had cerebral vasospasm, and 93 patients had insufficient cerebral blood supply (90.62%, including insufficient blood supply to the MCA and BA). Patients mainly with cerebral aneurysm and hypertensive intracerebral hemorrhage types contributed the highest proportion of insufficient blood supply, followed by the increase of blood flow, and the incidence of vasospasm was relatively low. In cerebral aneurysm group and hypertensive intracerebral hemorrhage group, and differences in the incidence of insufficient blood supply, increased blood flow, and vasospasm were statistically significant ( P<0.05). The bedside TCD monitoring can assess the patient's craniocerebral hemodynamic information and provide a clinical guidance.

Time course of coronary flow capacity impairment in ST-segment elevation myocardial infarction.

Microvascular dysfunction in the setting of ST-elevated myocardial infarction (STEMI) plays an important role in long-term poor clinical outcome. Coronary flow reserve (CFR) is a well-established physiological parameter to interrogate the coronary microcirculation. Together with hyperaemic average peak flow velocity, CFR constitutes the coronary flow capacity (CFC), a validated risk stratification tool in ischaemic heart disease with significant prognostic value. This mechanistic study aims to elucidate the time course of the microcirculation as reflected by alterations in microcirculatory physiological parameters in the acute phase and during follow-up in STEMI patients. We assessed CFR and CFC in the culprit and non-culprit vessel in consecutive STEMI patients at baseline (n = 98) and after one-week (n = 64) and six-month follow-up (n = 65). A significant trend for culprit CFC in infarct size as determined by peak troponin T (p = 0.004), time to reperfusion (p = 0.038), the incidence of final Thrombolysis In Myocardial Infarction 3 flow (p = 0.019) and systolic retrograde flow (p = 0.043) was observed. Non-culprit CFC linear contrast analysis revealed a significant trend in C-reactive protein (p = 0.027), peak troponin T (p < 0.001) and heart rate (p = 0.049). CFC improved both in the culprit and the non-culprit vessel at one-week (both p < 0.001) and six-month follow-up (p = 0.0013 and p < 0.001) compared with baseline. This study demonstrates the importance of microcirculatory disturbances in the setting of STEMI, which is relevant for the interpretation of intracoronary diagnostic techniques which are influenced by both culprit and non-culprit vascular territories. Assessment of non-culprit vessel CFC in the setting of STEMI might improve risk stratification of these patients following coronary reperfusion of the culprit vessel.

New insights to the potential mechanisms driving coronary flow reserve impairment in Cushing's syndrome: A pilot noninvasive study by transthoracic Doppler echocardiography

BackgroundThe contribution of functional and/or structural remodeling to reduced coronary flow velocity reserve (CFVR), reflecting impaired coronary microcirculation in Cushing's syndrome (CS), has not been clearly elucidated. We aimed to identify the potential mechanisms of coronary microvascular impairment in CS. MethodsWe studied 15 CS patients (11 female, age 50 ± 9 years) without clinical evidence of cardiovascular disease. Coronary flow velocity in the left anterior descending coronary artery was measured by transthoracic Doppler echocardiography, at rest, and during adenosine infusion. Average peak flow velocities, CFVR, and microvascular resistance in baseline (BMR) and hyperemic conditions (HMR) were assessed. CFVR ≤2.5 was considered a marker of microvascular disease (CMD). Diastolic function (E/e′), global longitudinal strain (GLS) and fractional pulse pressure (fPP), an index of arterial stiffness, were also assessed. ResultsCMD was present in 5 patients (33.3%). CMD was primarily driven by increased baseline peak flow velocity (29 ± 12 versus 19.6 ± 4.2 cm/s, p = .03) in the presence of decreased BMR (3.62 ± 0.6 versus 5.46 ± 1.4 mm Hg·s/cm, p = .03). Moreover, urinary cortisol and E/e′ were higher (p = .001 and p = .001, respectively) and GLS was lower (p = .009) in patients with CMD. fPP was higher in patients with CMD (p = .01). Urinary cortisol correlated to CFVR (p = .008), E/e′ (p < .0001) and GLS (p < .0001). fPP directly correlated to average peak flow velocities at rest (p = .01) and inversely to BMR (p = .03). ConclusionsFunctional microvascular regulatory impairment seems to be the potential mechanism of CMD in CS. CMD seems to be related to decreased myocardial contractility and diastolic dysfunction associated with cortisol excess.

Highlights From the Circulation Family of Journals.

Highlights From the Circulation Family of Journals.

Quantification of Myocardial Mass Subtended by a Coronary Stenosis Using Intracoronary Physiology.

In patients with stable coronary artery disease, the amount of myocardium subtended by coronary stenoses constitutes a major determinant of prognosis, as well as of the benefit of coronary revascularization. We devised a novel method to estimate partial myocardial mass (PMM; ie, the amount of myocardium subtended by a stenosis) during physiological stenosis interrogation. Subsequently, we validated the index against equivalent PMM values derived from applying the Voronoi algorithm on coronary computed tomography angiography. Based on the myocardial metabolic demand and blood supply, PMM was calculated as follows: PMM (g)=APV×D2×π/(1.24×10-3×HR×sBP+1.6), where APV indicates average peak blood flow velocity; D, vessel diameter; HR, heart rate; and sBP, systolic blood pressure. We calculated PMM to 43 coronary vessels (32 patients) interrogated with pressure and Doppler guidewires, and compared it with computed tomography-based PMM. Median PMM was 15.8 g (Q1, Q3: 11.7, 28.4 g) for physiology-based PMM, and 17.0 g (Q1, Q3: 12.5, 25.9 g) for computed tomography-based PMM (P=0.84). Spearman rank correlation coefficient was 0.916 (P<0.001), and Passing-Bablok analysis revealed absence of both constant and proportional differences (coefficient A: -0.9; 95% CI, -4.5 to 0.9; and coefficient B, 1.00; 95% CI, 0.91 to 1.25]. Bland-Altman analysis documented a mean bias of 0.5 g (limit of agreement: -9.1 to 10.2 g). Physiology-based calculation of PMM in the catheterization laboratory is feasible and can be accurately performed as part of functional stenosis assessment.

DIAGNOSTIC THRESHOLDS FOR CORONARY MICROVASCULAR DYSFUNCTION

Coronary microvascular dysfunction (MVD) is diagnosed when there is impaired coronary flow reserve (CFR) in the context of unobstructed arteries, but the optimum diagnostic threshold remains unclear. Patients with angina and unobstructed coronary arteries were enrolled. Average peak flow velocity (

ANGINA IS ASSOCIATED WITH CORONARY BLOOD FLOW - RESULTS FROM THE NHLBI-SPONSORED WOMEN'S ISCHEMIA SYNDROME EVALUATION: CORONARY VASCULAR DYSFUNCTION (WISE-CVD) PROJECT

Women with signs and symptoms of ischemia and non-obstructive coronary artery disease (INOCA) often have coronary microvascular dysfunction (CMD). We have previously observed that baseline average peak flow velocity (BAPV) is correlated with volumetric flow and predicted major adverse cardiovascular

Nailfold avascular score and coronary microvascular dysfunction in systemic sclerosis: A newsworthy association.

We aimed to assess the relationship between nailfold videocapillaroscopy (NVC) abnormalities and coronary flow reserve (CFR), a marker of coronary microvascular dysfunction (CMD) in patients with systemic sclerosis (SSc). We studied 39 SSc patients (33 females, mean ± SD age 54 ± 12 years, median disease duration 11 years, range 6-22) and 22 controls (matched for age and sex) without any evidence of cardiovascular disease. Clinical assessment was performed by modified Rodnan skin score (mRss) and EUSTAR score. Coronary flow velocities in the left anterior descending coronary artery were measured by transthoracic echocardiography. Average peak flow velocities, CFR and microvascular resistance at baseline (BMR) and in hyperaemic (HMR) condition were assessed. CFR ≤2.5 was considered marker of CMD. Six NVC-abnormalities were evaluated by a semi quantitative scoring system: enlarged and giant capillaries (diameter > 20 μm and >50 μm, respectively), hemorrhages, disarray, capillary ramifications and loss of capillaries (avascular score). Statistic was performed using SPSS. CFR was lower in SSc patients than in controls (2.6 ± 0.5 vs 3.3 ± 0.5). CMD was detected in 24 patients (61.5%) vs 0 controls (p < .0001). CFR was inversely correlated with NVC-avascular score (rho =-0.750, p < .0001). Avascular and capillary ramifications scores (p = .001 and p = .03, respectively), mRss (p = .003) and EUSTAR score (p = .01) were higher in patients with CMD than in those without. At multivariable analysis, avascular score was independently associated with CMD (p = .01). HMR was directly correlated with avascular score (rho = 0.416, p = .008). In our SSc patients NVC-avascular score was associated with CMD which seems to be the result of a structural microvascular remodeling.

Resting Coronary Flow Varies With Normal Cardiac Catheter Laboratory Stimuli.

Growing evidence supports physiology-guided revascularization, with Fractional Flow Reserve (FFR) the most commonly used invasive measure of coronary blood flow impairment at the time of diagnostic angiography. Recently, there has been growing interest in stenosis severity indices measured at rest, such as Instantaneous Wave Free Ratio (iFR) and the ratio of distal coronary to aortic pressure at rest (resting Pd/Pa). Their reliability may, theoretically, be more susceptible to changes in microvascular tone and coronary flow. This study aimed to assess variability of resting coronary flow with normal catheter laboratory stimuli. Simultaneous intracoronary pressure (Pd) and Doppler Average Peak Flow Velocity (APV) recordings were made at rest and following the verbal warning preceding an intravenous adenosine infusion. 72 patients undergoing elective angiography were recruited (mean age 62 years, 52.7% male) with a wide range of coronary artery disease severity (FFR 0.86 ± 0.09). Average peak flow velocity varied significantly between measurements at rest and just prior to commencement of adenosine, with a mean variation of 10.2% (17.82 ± 9.41 cm/s vs. 19.63 ± 10.44 cm/s, p < 0.001) with an accompanying significant drop in microvascular resistance (6.27 ± 2.73 mm Hg·cm-1·s-1 vs. 5.8 ± 2.92 mm Hg·cm-1·s-1, p < 0.001). These changes occurred without significant change in systemic hemodynamic measures. Whilst there was a trend for an associated change in the resting indices, Pd/Pa and iFR, this was statistically and clinically not significant (0.92 ± 0.08 vs. 0.92 ± 0.08, p = 0.110; and 0.90 ± 0.11 vs. 0.89 ± 0.12, p = 0.073). Resting coronary flow and microvascular resistance vary significantly with normal catheter laboratory stimuli, such as simple warnings. The clinical impact of these observed changes on indices of stenosis severity, particularly those measured at rest, needs further assessment within larger cohorts.

Bimodal Pattern of Coronary Microvascular Involvement in Diabetes Mellitus.

BackgroundThe contribution of functionally disturbed coronary autoregulation and structurally impaired microvascular vasodilatory function to reduced coronary flow velocity reserve, reflecting impaired coronary microcirculation in diabetes mellitus (DM), has not been clearly elucidated. The objective of this study was to identify the mechanism of coronary microvascular impairment in DM in relation to duration of disease.Methods and ResultsCoronary flow velocities in the anterior descending coronary artery were assessed by transthoracic echocardiography following angiography revealing normal epicardial coronary arteries in 55 diabetic and 47 nondiabetic patients. Average peak flow velocities, coronary flow velocity reserve, and microvascular resistance in baseline and hyperemic conditions (baseline and hyperemic microvascular resistance, respectively) were assessed. Reduced coronary flow velocity reserve in patients with short duration (<10 years) of DM compared with nondiabetic patients was primarily driven by increased baseline average peak flow velocity (26.50±5.6 versus 22.08±4.31, P=0.008) in the presence of decreased baseline microvascular resistance (3.69±0.86 versus 4.34±0.76, P=0.003). In contrast, decreased coronary flow velocity reserve in patients with long‐standing (≥10 years) DM compared with nondiabetic patients was predominantly driven by reduced hyperemic average peak flow velocity (41.57±10.01 versus 53.47±11.8, P<0.001) due to increased hyperemic microvascular resistance (2.13±0.42 versus 1.69±0.39, P<0.001).ConclusionsBoth altered coronary autoregulation and impaired microvascular vasodilatory function contribute to DM‐related coronary microvascular impairment in a time‐dependent manner. DM‐induced early functional microvascular autoregulatory impairment seems to evolve into structural microvascular impairment in the initially overperfused microvascular territory at the later stage of disease.

18 Baseline coronary flow varies with normal cardiac catheter laboratory stimuli: Abstract 18 Table 1

Introduction Fractional Flow Reserve (FFR) is a pressure-derived estimate of coronary flow impairment during maximal and constant hyperaemia provided by an adenosine infusion, when flow and pressure approximate linearly. The need for adenosine-induced hyperaemia has led to development of a stenosis severity index measured at rest, Instantaneous Wave Free Ratio (iFR). Its use and proposed applicability to serial/diffuse disease has relied on assumptions that coronary flow at rest is maintained at constant levels. This study aimed to assess variability of resting coronary flow with normal Catheter laboratory stimuli. Methods Forty-Seven elective patients were recruited with a variety of coronary artery disease severity (mean FFR: 0.883; SD: 0.938). Simultaneous intracoronary pressure (Pd) and Doppler Average Peak Flow Velocity, APV(U), recordings were made. These were made both at rest and just prior to supine bicycle exercise or intravenous adenosine infusion. Results Average peak flow velocity varied significantly between measurements at rest and just prior to commencement of adenosine or supine bicycle exercise (18.1765cm/s vs. 19.4689cm/s, p 0.002). This was without significant change in haemodynamics (Table 1). Conclusion Resting coronary flow appears to vary significantly with normal Catheter Laboratory stimuli, such as simple warnings, irrespective of haemodynamic status.

Diagnostic and Prognostic Implications ofCoronary Flow Capacity: A Comprehensive Cross-Modality Physiological Concept in Ischemic Heart Disease.

The purpose of this study is to evaluate whether coronary flow capacity (CFC) improves discrimination of patients at risk for major adverse cardiac events (MACE) compared with coronary flow reserve (CFR) alone, and to study the diagnostic and prognostic implications of CFC in relation to contemporary diagnostic tests for ischemic heart disease (IHD), including fractional flow reserve (FFR). Although IHD results from a combination of focal obstructive, diffuse, and microcirculatory involvement of the coronary circulation, its diagnosis remains focused on focal obstructive causes. CFC comprehensively documents flow impairment in IHD, regardless of its origin, by interpreting CFR in relation to maximal flow (hyperemic average peak flow velocity [hAPV]), and overcomes the limitations of using CFR alone. This is governed by the understanding that ischemia occurs in vascular beds with substantially reduced hAPV and CFR, whereas ischemia is unlikely when hAPV or CFR is high. Intracoronary pressure and flow were measured in 299 vessels (228 patients), where revascularization was deferred in 154. Vessels were stratified as having normal, mildly reduced, moderately reduced, or severely reduced CFC using CFR thresholds derived from published data and corresponding hAPV percentiles. The occurrence of MACE after deferral of revascularization was recorded during 11.9 years of follow-up (quartile 1: 10.0 years, quartile 3: 13.4 years). Combining CFR and hAPV improved the prediction of MACE over CFR alone (p= 0.01). After stratification in CFC, MACE rates throughout follow-up were strongly associated with advancing impairment of CFC (p= 0.002). After multivariate adjustment, mildly and moderately reduced CFC were associated with a 2.1-fold (95% confidence interval: 1.1 to 4.0; p= 0.017), and 7.1-fold (95% confidence interval: 2.9 to 17.1; p< 0.001) increase in MACE hazard, respectively, compared with normal CFC. Severely reduced CFC was identified by FFR≤0.80 in 90% of cases, although≥40% of vessels with normal or mildly reduced CFC still had an FFR≤0.80. CFC provides a cross-modality platform for the diagnosis and risk-stratification of IHD and enriches the interpretation of contemporary diagnostic tests in IHD.

Abstract 55: Histological And Rheological Evaluation At Coronary Artery Lesions In Patients With Kawasaki Disease Within 2 Years From Onset

Background: Some paper reported that intravascular ultrasound (IVUS)- virtual histology (VH) showed atherogenesis in the evolution of coronary artery lesions (CAL) in young adults long after Kawasaki disease(KD). However, there is no report about those findings during early phase of KD. Purpose: We perform coronary intimal histologic evaluation by IVUS-VH for KD patients with CAL within two years from onset. Furthermore, we calculate shear stress in the target site and examine whether rheological potential affects to vascular histological change after KD. Subjects and Methods: IVUS-VH was performed in 12 Japanese KD patients (median age, 5.1 years) during 2 years after onset of KD (median, 10.2months) . All these patients had giant aneurysm in another branches. We investigated 20 coronary branches including 10 sites of small aneurysm (s-AN), 10 sites of regressed s-AN, and 20 sites of normal segment. Each of the 4 plaque components was assigned a respective color and defined as follows: fibrous area (green); fibro-fatty area (yellow) ; necrotic core area (red); and dense calcium area (white). Moreover, we measured average coronary peak flow velocity by Flow wire and calculated shear stress in the each sites. Results: 10 sites of s-AN showed prominent endothelial hypertrophy with fibrous and/or fibro-fatty plaques. In 7 sites of these 10 sites, dense calcium and necrotic core localized which indicates early phase of atherosclerosis. 10 sites of regressed s-AN had circumferential endothelial hypertrophy occupying mainly fibrous and/or fibro-fatty plaques composition. In 8 sites of these regressed 10 sites, dense calcium and necrotic core locally existed. On the other hand, normal segment in 20 sites had no plaque in 19 sites and trivial plaque in 1 site. Moreover, shear stress in all evaluated VH sites were within normal limit, which shows rheological potential doesn’t affect to vascular remodeling in such coronary artery lesions. Conclusions: IVUS-VH study revealed that initial atherosclerotic findings locally existed not only at small aneurysm site but also at regressed site. Therefore, careful further investigation to vascular remodeling in KD patients with CAL including regressed s-AN will be need.

Prognostic Value of Microvascular Resistance Index Immediately After Primary Percutaneous Coronary Intervention on Left Ventricular Remodeling in Patients With Reperfused Anterior Acute ST-Segment Elevation Myocardial Infarction

This study sought to investigate the relationship between the degree of microvascular dysfunction assessed by a dual-sensor guidewire (pressure and Doppler velocity) and left ventricular (LV) remodeling after successful primary percutaneous coronary intervention (PPCI) for a first anterior acute myocardial infarction (AMI). Microvascular dysfunction after AMI is associated with progressive LV dilation. In 24 consecutive patients, the microvascular resistance index (MVRI) immediately after PPCI was calculated as the ratio of the mean distal pressure to average peak flow velocity during maximal hyperemia. Cardiac magnetic resonance was performed to determine LV volumes at baseline and 8-month follow-up. LV remodeling was defined as an increase in left ventricular end-diastolic volume (LVEDV) of ≥20%. In patients with an MVRI greater than the median value of 2.96 mm Hg·cm(-1)·s, the LVEDV increased significantly from 117.1 ± 20.7 ml at baseline to 146.5 ± 21.4 ml (p = 0.006) at 8 months, whereas it did not change between baseline and 8 months (108.2 ± 21.2 ml vs. 111.6 ± 29.9 ml, p = 0.620) in patients with an MVRI ≤2.96 mm Hg·cm(-1)·s. LV remodeling was more frequent in the group with an MVRI >2.96 mm Hg·cm(-1)·s (64% vs. 15%, p = 0.033). Furthermore, there was a positive correlation between MVRI and the percentage of increase or decrease in LVEDV (r = 0.42, p = 0.042). Logistic regression analysis showed that MVRI was the strongest univariate predictor of LV remodeling. The best cutoff value of MVRI was 2.96 mm Hg·cm(-1)·s with a sensitivity of 78% and a specificity of 73%. MVRI immediately after PPCI predicts LV remodeling in patients with reperfused anterior AMI.

Assessment of coronary microvascular resistance in the chronic infarcted pig heart

Pre-clinical studies aimed at treating ischemic heart disease (i.e. stem cell- and growth factor therapy) often consider restoration of the impaired microvascular circulation as an important treatment goal. However, serial in vivo measurement hereof is often lacking. The purpose of this study was to evaluate the applicability of intracoronary pressure and flow velocity as a measure of microvascular resistance in a large animal model of chronic myocardial infarction (MI). Myocardial infarction was induced in Dalland Landrace pigs (n = 13; 68.9 ± 4.1 kg) by a 75-min. balloon occlusion of the left circumflex artery (LCX). Intracoronary pressure and flow velocity parameters were measured simultaneously at rest and during adenosine-induced hyperemia, using the Combowire (Volcano) before and 4 weeks after MI. Various pressure- and/or flow-derived indices were evaluated. Hyperemic microvascular resistance (HMR) was significantly increased by 28% in the infarct-related artery, based on a significantly decreased peak average peak flow velocity (pAPV) by 20% at 4 weeks post-MI (P = 0.03). Capillary density in the infarct zone was decreased compared to the remote area (658 ± 207/mm2 versus 1650 ± 304/mm2, P = 0.017). In addition, arterioles in the infarct zone showed excessive thickening of the alpha smooth muscle actin (αSMA) positive cell layer compared to the remote area (33.55 ± 4.25 μm versus 14.64 ± 1.39 μm, P = 0.002). Intracoronary measurement of HMR successfully detected increased microvascular resistance that might be caused by the loss of capillaries and arteriolar remodelling in the chronic infarcted pig heart. Thus, HMR may serve as a novel outcome measure in pre-clinical studies for serial assessment of microvascular circulation.

Value of admission glucose to predict impaired coronary microcirculation in acute ST-elevation myocardial infarction

Background: Acute hyperglycemia is frequently observed in non-diabetic ST-elevation myocardial infarction (STEMI) patients. It is thought to be associated with the release of stress-mediators like noradrenalin and cortisol, which antagonize insulin and promote glycogenolysis and hyperglycemia, or with the high incidence of impaired glucose tolerance among STEMI patients. Hyperglycemia recently was shown to be associated with the no-reflow phenomenon, which is mainly a manifestation of microvascular dysfunction. We recently showed that no-reflow (or not achieving TIMI 3 flow) with primary PCI for STEMI had independent prognostic value with regard tot 30-day, as well as 1-year mortality, next to admission glucose. Although no reflow in this study was an indirect measure of microvascular dysfunction, the significant association between no-reflow and increasing admission glucose and the attenuation of the effect of no-reflow by glucose concentration in multivariate analysis indicate the role of acute hyperglycemia in the pathophysiology of microvascular dysfunction. Methods: In 76 patients with a first anterior wall STEMI, baseline and minimal microvascular resistance in IRAs and non-IRAs immediately after reperfusion and at 1-week and 6-month follow-up were calculated as the ratio of mean transvascular pressure gradient to mean baseline and to adenosine-induced hyperemic blood flow velocity, respectively. Patients were divided in two groups, glucose below 11.0 mmol/L (group A) and glucose equal or higher than 11 mmol/L (group B), according to a cut-off level of the American Diabetes Association and the Euro Heart Survey. Results: Minimum microvascular resistance, defined as the ratio of mean distal pressure to average peak blood flow velocity during maximum hyperemia, showed a large variability (overall range, 0.75 to 4.89 mm Hg cm-1 s-1) and was significantly higher in group B than in group A immediately after reperfusion and at 1-week. Conclusion: In conclusion, minimal microvascular resistance is higher in anterior STEMI patients with hyperglycemia equal or above 11.0 mmol/L compared to patients with glucose leven lower than 11.0 mmol/L. Hyperglycemia in STEMI patients could prove to be an important predictor of microvacular dysfunction and obstruction.