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OBJECTIVE: Bicuspid aortic valve (BAV) is the most common congenital heart defect. Ascending aorta dilatation is related to BAV- and hypertension (HTN)-associated aortopathy. The aim of this study was to investigate aortic elasticity, as well as aortic deformation of the ascending aorta, using strain imaging, and to evaluate the possible relationship of biomarkers, such as endotrophin and matrix metalloproteinase-2 (MMP-2), with ascending aorta dilatation in patients with BAV- or HTN-associated aortopathy. PATIENTS AND METHODS: This prospective study included patients with ascending aorta dilatation with BAV (n = 33), or normal tricuspid aortic valve with HTN (n = 33), and 20 control subjects. The mean age of the total patients was 42.76 ± 10.4 years (67% male, 33% female). We calculated aortic elasticity parameters using the relevant formula by M-mode echocardiography and determined layer-specific longitudinal and transverse strains of the proximal aorta by speckle-tracking echocardiography. Blood samples of the participants were drawn for the analysis of endotrophin and MMP-2. RESULTS: Aortic strain and aortic distensibility were significantly decreased, whereas the aortic stiffness index was significantly increased in patient groups with BAV or HTN compared to the control group (p < 0.001). Moreover, longitudinal strain of both the anterior and posterior aortic walls of the proximal aorta were significantly impaired in BAV and HTN patients (p < 0.001). Serum endotrophin levels were significantly reduced in the patient cohort compared to the controls (p = 0.001). Endotrophin was noted to be significantly positively correlated with aortic strain and aortic distensibility (r = 0.37, p = 0.001; r = 0.45, p < 0.001, respectively), whereas inversely associated with aortic stiffness index (r = -0.402, p < 0.001). Furthermore, endotrophin was the single independent predictor of ascending aorta dilatation (OR = 0.986, p < 0.001). A cut-off value of endotrophin = 82.38 ng/mL predicted ascending aorta dilatation with a sensitivity of 80.3% and specificity of 78.5% (p < 0.0001). CONCLUSIONS: The present study showed that aortic deformation parameters and elasticity are impaired in BAV and HTN patients, and strain imaging allows for a good analysis of ascending aorta deformation. Endotrophin could be a predictive biomarker of ascending aorta dilatation in BAV and HTN aortopathy. [ABSTRACT FROM AUTHOR]

Considering that coronary artery disease (CAD) is the number one cause of death in the developed countries and higher than half of patients with severe clinical symptoms do not have any predictive sign for CAD necessitate the development of advanced screening tests. Coronary artery calcium score (CCS) test depending on the principle of measurement of calcium level in atherosclerotic lesions is one of the most important steps in this field. Coronary artery calcification is recognized as an active process that is closely linked to vascular inflammation and predicts future cardiac events. Presence of calcium in vascular lesions allows us to assess the lesion burden. Nowadays spiral CT is being widely used to define structural changes and calcium deposition in coronary artery segments instead of electron beam tomography which is initially used. However, since there are numerous non-calcified lipid-rich plaques with thin fibrous caps besides calcified plaques in CAD patients, CCS is not efficient test to evaluate the risk of CAD alone. The CCS percentiles defined for age and gender are more relevant in assessing risk and more predictive of hard cardiac events than absolute CCS. In asymptomatic cases, while being zero of CCS do not eliminate the risk of occurring acute cardiac events and the possibility of myocardial ischemia, the presence of high CCS rises predictive value of Framingham risk score (FRS) for coronary death and non-fatal myocardial infarction. Finally, the CCS is valuable test screening tool in selected patients such as those with an intermediate FRS, as recommended by the current guidelines; high coronary calcium score is closely related with the increased risk of CAD and serious cardiac events, and signs to requirement for secondary prevention and other advanced techniques in the diagnosis of CAD. [ABSTRACT FROM AUTHOR]

Coronary microvascular vasodilator capacity is substantially associated with coronary pressure waveform and dicrotic notch morphology, with or without concomitant epicardial disease. A prominent dicrotic notch is associated with preserved microvascular vasodilatory capacity and adequate resting microvascular tonus without relative hyperaemic state, cumulatively indicating a better microcirculatory health., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Coronary microvascular dysfunction (CMD) is the leading cause of ischemia with no obstructive coronary arteries disease (INOCA) disease. Diagnosis of CMD relies on surrogate physiological indices without objective proof of ischemia., Objectives: Intracoronary electrocardiogram (icECG) derived hyperemic indices may accurately and objectively detect CMD and reversible ischemia in related territory., Methods: INOCA patients with proven ischemia by myocardial perfusion scan (MPS) and completely normal coronary arteries underwent simultaneous intracoronary electrophysiological (icECG) and physiological (intracoronary Doppler) assessment in all 3 coronary arteries during rest and under adenosine induced hyperemia., Results: Sixty vessels in 21 patients were included in the final analysis. All patients had at least one vessel with abnormal CFR. 41 vessels had CMD (CFR < 2.5), of which 26 had increased microvascular resistance (structural CMD, HMR > 1.9 mmHg.cm -1 .s) and 15 vessels had CMD (CFR < 2.5) with normal microvascular resistance (functional CMD, HMR <= 1.9 mmHg.cm -1 .s). Only one-third of the patients (n = 7) had impaired CFR < 2.5 in all 3 epicardial arteries. Absolute ST shift between hyperemia and rest (∆ST) has shown the best diagnostic performance for ischemia (cut-off 0.10 mV, sensitivity: 95%, specificity: 72%, accuracy: 80%, AUC: 0.860) outperforming physiological indices (CFR: 0.623 and HMR: 0.653 DeLong's test P = .0002)., Conclusions: In INOCA patients, CMD involves coronary artery territories heterogeneously. icECG can accurately detect CMD causing perfusion abnormalities in patients with INOCA outperforming physiological CMD markers, by demonstrating actual ischemia instead of predicting the likelihood of inducible ischemia based on violated surrogate thresholds of blunted flow reserve or increased minimum microvascular resistance., Condensed Abstract: In 21 INOCA patients with coronary microvascular dysfunction (CMD) and myocardial perfusion scan proved ischemia, hyperemic indices of intracoronary electrocardiogram (icECG) have accurately detected vessel-specific CMD and resulting perfusion abnormalities & ischemia, outperforming invasive hemodynamic indices. Absolute ST shift between hyperemia and rest (∆ST) has shown the best classification performance for ischemia in no Obstructive Coronary Arteries (AUC: 0.860) outperforming Doppler derived CMD indices (CFR: 0.623 and HMR: 0.653 DeLong's test P = .0002).icECG can be used to diagnose CMD causing perfusion defects by demonstrating actual reversible ischemia at vessel-level during the initial CAG session, obviating the need for further costly ischemia tests., Clinicaltrials: GOV: NCT05471739., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Objective: The growing incidence of diabetes and the increasing life expectancy of the diabetic population worldwide has increased the number of diabetic vascular complications occurring in cardiology practice. As current treatment and prevention methods are less effective in this patient group, there is a need for new treatment methods in this area. Exercise, which reduces metabolic and vascular problems associated with diabetes, often becomes impossible, especially in advanced-stage patients who need exercise the most. Since exercise and flow-mediated dilation (FMD) are effective by stimulating mechanotransduction mechanisms on the endothelium, it can be expected that the same mechanisms could also be stimulated by direct vibration., Methods: In order to test this hypothesis, in this study, a group of 20 type 2 diabetes patients (11 males, age 56.80 ± 11.05 years and diagnosed for 15.35 ± 8.61 years) were examined via the application of FMD and vibration-mediated dilation (VMD). We performed vibration for five minutes with 20-Hz frequency and 3-mm vertical amplitude, to the same side forearm, with a 30-minute interval. Using a 10-MHz linear echo probe, brachial artery diameter and flow velocities were recorded for 10 minutes before and at two-minute intervals after the FMD and VMD applications. Then brachial artery flow and resistance were calculated at each stage., Results: In the first minute after FMD and VMD applications, brachial artery diameter and flow velocities increased significantly, and vascular resistance decreased significantly. None of the corresponding FMD or VMD parameters in the first minute was different. The artery diameters in the first minute after FMD and VMD were increased by 6.04 ± 5.29 and 5.49 ± 5.21%, respectively. At the tenth minute, these values decreased to 1.73 ± 3.21 and 2.05 ± 3.31%. In the FMD series, all parameters except brachial artery diameter returned to their baseline values after the fourth minute. After VMD, all parameters also decreased after the first minute, but the recovery was much slower. At each stage after the first minute, the VMD averages were higher than the baseline value and their corresponding FMD values., Conclusion: The results of this study indicated that vibration may be a powerful, long-lasting and feasible treatment option in patients with peripheral perfusion failure, developed due to diabetic macro- and microvascular complications.

Background: Although there are studies examining each one separately, there are no data in the literature comparing the magnitudes of the iatrogenic, percutaneous coronary intervention (PCI)-induced, microvascular dysfunction (Type-4 CMD) and coronary microvascular dysfunction (CMD) in the setting of ischaemia in non-obstructed coronary arteries (INOCA) (Type-1 CMD)., Objectives: We aimed to compare the characteristics of Type-1 and Type-4 CMD subtypes using coronary haemodynamic (resistance and flow-related parameters), thermodynamic (wave energy-related parameters) and hyperemic ECG changes., Methods: Coronary flow reserve (CFR) value of <2.5 was defined as CMD in both groups. Wire-based multimodal perfusion markers were comparatively analysed in 35 patients (21 INOCA/CMD and 14 CCS/PCI) enrolled in NCT05471739 study., Results: Both groups had comparably blunted CFR values per definition (2.03±0.22 vs 2.11±0.37; p: 0.518) and similar hyperemic ST shift in intracoronary ECG (0.16±0.09 vs 0.18±0.07 mV; p: 0.537). While the Type-1 CMD was characterised with impaired hyperemic blood flow acceleration (46.52+12.83 vs 68.20+28.63 cm/s; p: 0.017) and attenuated diastolic microvascular decompression wave magnitudes (p=0.042) with higher hyperemic microvascular resistance (p<0.001), Type-4 CMD had blunted CFR mainly due to higher baseline flow velocity due to post-occlusive reactive hyperemia (33.6±13.7 vs 22.24±5.3 cm/s; p=0.003)., Conclusions: The perturbations in the microvascular milieu seen in CMD in INOCA setting (Type-1 CMD) seem to be more prominent than that of seen following elective PCI (Type-4 CMD), although resulting reversible ischaemia is equally severe in the downstream myocardium., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: There is an ongoing debate on the extension of reperfusion-related microvascular damage (MVD) throughout the remote noninfarcted myocardial regions in patients with ST-elevation myocardial infarction (STEMI) that undergo primary percutaneous intervention (pPCI). The aim of this study was to elucidate the impact of reperfusion on remote microcirculatory territory by analyzing hemodynamic alterations in the nonculprit-vessel in relation to reperfusion., Methods: A total of 20 patients with STEMI undergoing pPCI were included. Peri-reperfusion temporal changes in hemodynamic parameters were obtained in angiographically normal nonculprit vessels before and 1-h after reopening of the culprit vessel. Intracoronary pressure and flow velocity data were compared using pairwise analyses (before and 1-h after reperfusion)., Results: In the non-culprit vessel, compared to the pre-reperfusion state, mean resting average peak velocity (33.4 ± 9.4 to 25.0 ± 4.9 cm/s, P < 0.001) and mean hyperemic average peak velocity (53.5 ± 14.4 to 42.1 ± 10.66 cm/s, P = 0.001) significantly decreased; whereas baseline (3.2 ± 1.0 to 4.0 ± 1.0 mmHg.cm -1 .s, P < 0.001) and hyperemic microvascular resistance (HMR) (1.9 ± 0.6 to 2.4 ± 0.7 mmHg.cm -1 .s, P < 0.001) and mean zero flow pressure (Pzf) values (32.5 ± 6.9 to 37.6 ± 8.3 mmHg, P = 0.003) significantly increased 1-h after reperfusion. In particular, the magnitude of changes in HMR and Pzf values following reperfusion were more prominent in patients with larger infarct size and with higher extent of MVD in the culprit vessel territory., Conclusion: Reperfusion-related microvascular injury extends to involve remote myocardial territory in relation to the magnitude of the adjacent infarction and infarct-zone MVD. (GUARD Clinical TrialsNCT02732080)., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion-related microvascular damage in ST-segment-elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by primary percutaneous coronary intervention. We investigated whether pressure-controlled reperfusion via gradual reopening of the infarct-related artery may limit microvascular injury in patients undergoing primary percutaneous coronary intervention. Methods and Results A total of 83 patients with ST-segment-elevation myocardial infarction were assessed for eligibility and 53 who did not meet inclusion criteria were excluded. The remaining 30 patients with totally occluded infarct-related artery were randomized to the pressure-controlled reperfusion with delayed stenting (PCRDS) group (n=15) or standard primary percutaneous coronary intervention with immediate stenting (IS) group (n=15) (intention-to-treat population). Data from 5 patients in each arm were unsuitable to be included in the final analysis. Finally, 20 patients undergoing primary percutaneous coronary intervention who were randomly assigned to either IS (n=10) or PCRDS (n=10) were included. In the PCRDS arm, a 1.5-mm balloon was used to achieve initial reperfusion with thrombolysis in myocardial infarction grade 3 flow and, subsequently, to control distal intracoronary pressure over a 30-minute monitoring period (MP) until stenting was performed. In both study groups, continuous assessment of coronary hemodynamics with intracoronary pressure and Doppler flow velocity was performed, with a final measurement of zero flow pressure (primary end point of the study) at the end of a 60-minute MP. There were no complications associated with IS or PCRDS. PCRDS effectively led to lower distal intracoronary pressures than IS over 30 minutes after reperfusion (71.2±9.37 mm Hg versus 90.13±12.09 mm Hg, P =0.001). Significant differences were noted between study arms in the microcirculatory response over MP. Microvascular perfusion progressively deteriorated in the IS group and at the end of MP, and hyperemic microvascular resistance was significantly higher in the IS arm as compared with the PCDRS arm (2.83±0.56 mm Hg.s.cm -1 versus 1.83±0.53 mm Hg.s.cm -1 , P =0.001). The primary end point (zero flow pressure) was significantly lower in the PCRDS group than in the IS group (41.46±17.85 mm Hg versus 76.87±21.34 mm Hg, P =0.001). In the whole study group (n=20), reperfusion pressures measured at predefined stages in the early reperfusion period showed robust associations with zero flow pressure values measured at the end of the 1-hour MP (immediately after reperfusion: r =0.782, P <0.001; at the 10th minute: r =0.796, P <0.001; and at the 20th minute: r =0.702, P =0.001) and peak creatine kinase MB level (immediately after reperfusion: r =0.653, P =0.002; at the 10th minute: r =0.597, P =0.007; and at the 20th minute: r =0.538, P =0.017). Enzymatic myocardial infarction size was lower in the PCRDS group than in the IS group with peak troponin T (5395±2991 ng/mL versus 8874±1927 ng/mL, P =0.006) and creatine kinase MB (163.6±93.4 IU/L versus 542.2±227.4 IU/L, P <0.001). Conclusions In patients with ST-segment-elevation myocardial infarction, pressure-controlled reperfusion of the culprit vessel by means of gradual reopening of the occluded infarct-related artery (PCRDS) led to better-preserved coronary microvascular integrity and smaller myocardial infarction size, without an increase in procedural complications, compared with IS. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02732080.

Objective: The aim of this cross-sectional, retrospective, descriptive study was to review and classify cardiac masses systematically and to determine their frequencies., Methods: The medical records of 64,862 consecutive patients were investigated within 12 years. Every patient with a cardiac mass imaged by transthoracic echocardiography (TTE) and confirmed with an advanced imaging modality such as transesophageal echocardiography (TEE), computed tomography (CT) and/or cardiac magnetic resonance imaging (CMR) was included. Acute coronary syndromes triggering thrombus formation, vegetations, intracardiac device and catheter related thrombi were excluded., Results: Data demonstrated 127 (0.195%) intracardiac masses consisting of 33 (0.050%) primary benign, 3 (0.004%) primary malignant, 20 (0.030%) secondary tumors, 3 (0.004%) hydatid cysts and 68 (0.104%) thrombi respectively. The majority of primary cardiac tumors were benign (91.67%), predominantly myxomas (78.79%), and the less malignant (8.33%). Secondary cardiac tumors were common than the primary malignant tumors (20:3), with male dominancy (55%), lymphoma and lung cancers were the most frequent. Intracardiac thrombi was the majority of the cardiac masses, thrombi accompanying malignancies were in the first range (n = 17, 25%), followed by autoimmune diseases (n = 13, 19.12%) and ischemic heart disease with low ejection fraction (n = 12, 17.65%)., Conclusions: This retrospective analysis identified 127 patients with cardiac masses. The majority of benign tumors were myxoma, the most common tumors that metastasized to the heart were lymphoma and lung cancers, and the thrombi associated with malignancies and autoimmune diseases were the most frequent., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 Published by Elsevier Inc.)

Fractional flow reserve (FFR) may not be immune from hemodynamic perturbations caused by both vessel and lesion related factors. The aim of this study was to investigate the impact of plaque- and vessel wall-related features of vulnerability on the hemodynamic effect of intermediate coronary stenoses. Methods and Results: In this cross-sectional study, patients referred to catheterization laboratory for clinically indicated coronary angiography were prospectively screened for angiographically intermediate stenosis (50-80%). Seventy lesions from 60 patients were evaluated. Mean angiographic stenosis was 62.1 ± 16.3%. After having performed FFR assessment, intravascular ultrasound (IVUS) was performed over the FFR wire. Virtual histology IVUS was used to identify the plaque components and thin cap fibroatheroma (TCFA). TCFA was significantly more frequent (65 vs. 38%, p = 0.026), and necrotic core volume (26.15 ± 14.22 vs. 16.21 ± 8.93 mm3, p = 0.04) was significantly larger in the positively remodeled than non-remodeled vessels. Remodeling index correlated with necrotic core volume (r = 0.396, p = 0.001) and with FFR (r = -0. 419, p = 0.001). With respect to plaque components, only necrotic core area (r = -0.262, p = 0.038) and necrotic core volume (r = -0.272, p = 0.024) were independently associated with FFR. In the multivariable model, presence of TCFA was independently associated with significantly lower mean FFR value as compared to absence of TCFA (adjusted, 0.71 vs. 0.78, p = 0.034). Conclusion: The current study demonstrated that for a given stenosis geometry, features of plaque vulnerability such as necrotic core volume, TCFA, and positive remodeling may influence the hemodynamic relevance of intermediate coronary stenoses., (© 2020 S. Karger AG, Basel.)

Background The extent of pressure-related damage might be related to acceleration rate of the applied pressure (peak dP/dt) in the vascular system. In this study, we sought to determine whether dP/dt applied to the aortic wall (aortic dP/dt) and in turn vascular extracellular matrix degradation can be mitigated via modulation of left ventricular (LV) contractility (LV dP/dt) by pacemaker-mediated desynchronization. Methods and Results First, in 34 patients, changes in aortic dP/dt values in 3 aortic segments in response to pacemaker-mediated stepwise QRS widening leading to gradual desynchronization of the LV contraction by means of steadily changed atrioventricular delay (AVD) with temporary dual-chamber pacing was examined before and after beta-blocker (15 mg IV metoprolol) administration. Second, serum matrix metalloproteinase-9 levels were measured in the 20 patients with permanent pacemaker while they were on sinus rhythm with normal QRS width and 3 weeks after wide QRS rhythm ensured by dual pacing, dual sensing, and dual response to sensing with short AVD. LV dP/dt substantially correlated with dP/dt measured in ascending ( r =0.83), descending ( r =0.89), and abdominal aorta ( r =0.96). QRS width strongly correlated with dP/dt measured in ascending ( r =-0.95), descending ( r =-0.92), and abdominal ( r =-0.96) aortic segments as well. In patients with permanent pacemaker, wide QRS rhythm led to a significant reduction in serum matrix metalloproteinase-9 levels (from 142.5±32.9 pg/mL to 87.5±32.4 pg/mL [ P <0.001]) at the end of 3 weeks follow-up. Conclusions QRS prolongation by short AVD dual pacing, dual sensing, and dual response to sensing results in concomitant decreases in peak dP/dt values in the LV and in all aortic segments with or without background beta-blocker administration, which in turn led to a significant reduction in circulating matrix metalloproteinase-9 levels. Registration URL: https://www.clini​caltr​ials.gov; Unique identifier: NCT03665558.

Objectives: Early detection of microvascular dysfunction after acute myocardial infarction (AMI) could identify patients at high risk of adverse clinical outcome, who may benefit from adjunctive treatment. Our objective was to compare invasively measured coronary flow reserve (CFR) and hyperaemic microvascular resistance (HMR) for their predictive power of long-term clinical outcome and cardiac magnetic resonance (CMR)-defined microvascular injury (MVI)., Methods: Simultaneous intracoronary Doppler flow velocity and pressure measurements acquired immediately after revascularisation for AMI from five centres were pooled. Clinical follow-up was completed for 176 patients (mean age 60±10 years; 140(80%) male; ST-elevation myocardial infarction (STEMI) 130(74%) and non-ST-segment elevation myocardial infarction 46(26%)) with median follow-up time of 3.2 years. In 110 patients with STEMI, additional CMR was performed., Results: The composite end point of death and hospitalisation for heart failure occurred in 17 patients (10%). Optimal cut-off values to predict the composite end point were 1.5 for CFR and 3.0 mm Hg cm -1 •s for HMR. CFR <1.5 was predictive for the composite end point (HR 3.5;95% CI 1.1 to 10.8), but not for its individual components. HMR ≥3.0 mm Hg cm -1 s was predictive for the composite end point (HR 7.0;95% CI 1.5 to 33.7) as well as both individual components. HMR had significantly greater area under the receiver operating characteristic curve for MVI than CFR. HMR remained an independent predictor of adverse clinical outcome and MVI, whereas CFR did not., Conclusions: HMR measured immediately following percutaneous coronary intervention for AMI with a cut-off value of 3.0 mm Hg cm -1 s, identifies patients with MVI who are at high risk of adverse clinical outcome. For this purpose, HMR is superior to CFR., Competing Interests: Competing interests: GAdW, DP, RK and NvR have received speaking/advisory board honoraria from Volcano Corporation. The other authors report no conflicts of interest pertaining to this study., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objective: The histological characteristics of plaque may affect the hemodynamic outcome of a given coronary stenosis. In particular, the potential effect of volumetric calcium content and the topographical distribution in the lesion segment on physiological outcome has not yet been investigated. The aim of this study was to identify any potential correlation between patterns of calcification and the fractional flow reserve (FFR) and the coronary remodeling index (RMI)., Methods: A total of 26 stable angina pectoris and 34 acute coronary syndrome patients without persistent ST-segment elevation constituted the study population. FFR was used to assess 70 intermediate coronary stenosis lesions. After obtaining hemodynamic measurements, quantitative grayscale and virtual histology-intravascular ultrasound analyses were performed. The depth, length, and circumferential distribution of calcification of the lesions were also recorded., Results: Within the analyzed segment (area of interest, lesion segment), FFR was correlated with maximal thickness of deep calcification (r=-0.285; p=0.021) and calcification angle (r=-0.396; p=0.001). In lesions with a calcification angle >180°, the mean FFR value was significantly lower compared with those <180° (0.64±0.17 vs. 0.78±0.08; p=0.024). RMI was correlated with maximal angle of superficial (r=-0.437; p<0.001) and deep (r=0.425; p<0.001) calcification. RMI was correlated with maximal thickness of superficial (r=-0.357; p=0.003) and deep (r=0.417; p<0.001) calcification. RMI was also correlated with FFR (r=-0.477; p<0.001)., Conclusion: This study demonstrated that the geometry, location, and amount of calcification of a plaque could affect hemodynamic and anatomical outcome measures in functionally significant stenoses by affecting vessel wall compliance.

Coronary microvascular dysfunction, also known as cardiac syndrome X, is a clinical syndrome presenting with typical angina and evidence of myocardial ischemia in the absence of flow-limiting stenosis on coronary angiography. Of patients undergoing coronary angiography due to suspected myocardial ischemia, 50% are found to have normal or near-normal coronary arteries. Described in this case report is a patient who developed hypotension and ST segment depressions during treadmill exercise test. Left main coronary artery or multivessel disease was suspected. Coronary angiography was normal, but coronary flow reserve measurement revealed severe microvascular dysfunction.

Background: The 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 Results: Coronary 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)., Conclusions: Both 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., (© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

High blood pressure (BP) has been identified as a major risk factor for cardiovascular complications. Although two-way association between BP and hypertensive complications makes hypertension a near-ideal biomarker, BP as "the cause" for the complications of HT per se still needs more evidence. Another entirely possible hemodynamic candidate for causing hypertensive cardiovascular adverse events can be flow or its iterations, which might have escaped the attention because of its perfect correlation with pressure and harder technical measurement. In this article, we analyze the evidence in hand to compare flow- and pressure-related phenomena to delineate which of the two is the dominant mediator of complications related to hypertension and should be the target for therapy. A "flow-" rather than a "pressure-" based factor, as the causative or major driving mediator of common hypertensive complications, may change our understanding of hypertension pathophysiology.

Objective: It is widely known that myocardial damage is not immediately terminated after the elimination of epicardial occlusion in cases of myocardial infarction. In situ thrombosis during epicardial occlusion might contribute to poor myocardial perfusion after reperfusion of an occluded epicardial artery. In the current study, we sought to determine the effects of ischemia and reperfusion on microvascular thrombotic occlusion., Methods: Thirty male Wistar rats were included in the study. After the rats had been anesthetized and thoracotomized, the left coronary artery was occluded for 30 minutes in the first group, and it was occluded for 30 minutes and reperfused for an additional 20 minutes in the second group. Ten rats were used as a sham-operated control group. After completion of the study protocol, excised heart preparations were analyzed by immunohistochemistry and electron microscopy., Results: A significant difference was found between the infarction plus reperfusion group and the other 2 groups, with respect to microvascular fibrin and thrombocyte deposition in immunohistochemistry analysis. These results were confirmed by morphological examination with electron microscopy., Conclusion: In situ fibrin formation accompanies microvascular obstruction in acute myocardial infarction. Our results indicate that additional therapeutic approaches are needed in order to achieve better tissue perfusion in contemporary treatment of acute myocardial infarction after successful reopening of the infarct-related artery.

Objective: Histologic plaque characteristics may influence the hemodynamic effect generated by physiologically significant unstable coronary lesions where plaque content and surface related factors are expected to contribute to the maximum translesional pressure drop. In this study, we aimed to identify local lesion specific virtual histological characteristics that may potentially affect hemodynamic outcome measures., Methods: Forty-eight consecutive patients with non-ST-elevation acute coronary syndrome (NSTEACS) having paired hemodynamic and morphological data were enrolled. A dual sensor guide-wire was used for the assessment of fractional flow reserve (FFR) and stenosis resistance (HSR) in the culprit vessel. Virtual histology intravascular ultrasound imaging was performed after obtaining hemodynamic data., Results: In a hemodynamically significant lesion subset (FFR<0.75 [n=34]), after controlling for lesion length, MLA and coronary artery compliance, FFR correlated with necrotic core (NC) area (r=-0.423, p=0.028) at MLA and NC volume (r=-0.497, p=0.008) and dense calcium (DC) volume (r=-0.332, p=0.03) across the entire lesion segment. Likewise, NC (r=-0.544, p=0.005) and DC (r=0.376, p=0.03) areas at MLA and NC (r=0.545, p=0.005) and DC (r=0.576, p=0.003) volumes across the entire lesion segment were associated with HSR in the hemodynamically significant lesion group (HSR>0.80 [n=33]). However, no correlation has been observed between intracoronary hemodynamic end-points and plaque components in hemodynamically insignificant lesions., Conclusions: This study demonstrated that for a given coronary stenosis geometry and arterial compliance, plaque composition may influence hemodynamic outcome measures in functionally significant stenoses in patients with NSTEACS., (Copyright © 2015. Published by Elsevier Ireland Ltd.)

Aims: In the acute coronary syndrome setting, the interaction between epicardial coronary artery stenosis and microcirculation subtended by the culprit vessel is poorly understood. The purpose of the present study was to assess the immediate impact of percutaneous coronary intervention (PCI) on microvascular resistance (MR) in patients with non-ST-elevation myocardial infarction (NSTEMI)., Methods and Results: Thirty-eight patients undergoing PCI for NSTEMI were recruited consecutively. Culprit lesions were stented over a Doppler and pressure-sensor-equipped guidewire. In the presence of epicardial stenosis, MR was calculated by taking collateral flow, as measured by the coronary wedge pressure, into consideration. After removal of epicardial stenosis, MR was calculated simply as distal coronary pressure divided by average peak velocity. When collateral flow was incorporated into the calculation, MR increased significantly from 1.70 ± 0.76 to 2.05 ± 0.72 (p=0.001) after PCI in the whole population. Periprocedural changes (Δ) in absolute values of MR and troponin T correlated significantly (r=0.629, p=0.0001). In patients who developed periprocedural myocardial infarction, MR increased significantly after PCI (1.48 ± 0.73 versus 2.28 ± 0.71, p<0.001). Nevertheless, removal of the epicardial lesion did not change MR in patients without periprocedural MI (1.91±0.73 versus 1.81±0.67, p=0.1)., Conclusions: When collateral flow is accounted for, removal of epicardial stenosis increases MR in patients with NSTEMI undergoing PCI.

The extent of coronary microvascular dysfunction might be related, not only to patient characteristics and procedural factors, but also to the inflammatory status. The aim of the present study was to examine a possible association between inflammation, as reflected by the serum C-reactive protein (CRP) levels, and the extent of baseline and post-percutaneous coronary intervention (PCI) coronary microvascular dysfunction in patients with non-ST-segment elevation acute coronary syndrome undergoing PCI. A total of 42 patients undergoing PCI for non-ST-segment elevation acute coronary syndrome were enrolled. Coronary microvascular resistance (MR) was determined in the territory of culprit artery using a Doppler probe- and a pressure sensor-equipped guidewire both before (taking the collateral blood into account) and after PCI. The periprocedural changes in MR were calculated. The CRP levels at admission were correlated with the pre-PCI MR (r = 0.498, p = 0.001), post-PCI MR (r = 0.429, p = 0.005), and periprocedural changes in MR (r = 0.785, p <0.001). On multivariate regression analysis, the only predictor of the pre-PCI (β = 0.531, p = 0.002) and post-PCI (β = 0.471, p = 0.012) MR was the serum CRP concentration. Likewise, the periprocedural changes in MR was predicted by the serum CRP levels (β = 0.677, p = 0.001) and the presence of angiographic thrombus (β = -0.275, p = 0.02). In conclusion, these results have shown that the CRP level is related to increased coronary MR in the territory of the culprit lesion. This suggests that inflammatory processes might play a role in microvascular impairment in patients with non-ST-segment elevation acute coronary syndrome., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Tirofiban is a glycoprotein (GP) IIb/IIIa receptor antagonist used in the treatment of acute coronary syndrome (ACS). Thrombocytopenia is a well-known complication of GPIIb/IIIa inhibitors. Life-threatening complications such as alveolar and gastrointestinal system hemorrhages may occur in the course of thrombocytopenia. Platelet count should be monitored closely, including during the first few hours of the infusion. Adverse events may be prevented by prompt discontinuation of the therapy. Herein we present two cases of profound and sudden thrombocytopenia associated with tirofiban use in the treatment of ACS together with a review of the literature.

Wolff-Parkinson-White (WPW) syndrome is a disorder characterized by presence of an accessory pathway that predisposes patients to tachyarrhythmias and sudden death. Radiofrequency ablation (RFA) is both effective and safe for patients with symptomatic tachyarrhythmias mediated by accessory atrioventricular pathways. During the procedure, fatal complications may occur but it is considered low in relation to the morbidity associated with the WPW syndrome. Coronary artery occlusion, as a complication of an RF catheter ablation, is quite rare. In this report, we present a 56-year-old male patient with a left main coronary artery (LMCA) occlusion during the ablation of left anterolateral wall accessory pathway. It should be kept in mind if the patient complains of new onset of severe chest pain, an immediate angiography should be performed., (©2010, The Authors. Journal compilation ©2012 Wiley Periodicals, Inc.)

Background: Connection between the course of microvascular and infarct remodeling processes over time after reperfused ST-elevation acute myocardial infarction has not been fully elucidated. The aim of this study is to investigate the association of temporal changes in hemodynamics of microcirculation in the infarcted territory and infarct size (IS) after primary percutaneous coronary intervention in patients with ST-elevation acute myocardial infarction., Methods and Results: Thirty-five patients admitted with ST-elevation acute myocardial infarction undergoing primary percutaneous coronary intervention were enrolled in the study. Coronary flow reserve (CFR), index of microvascular resistance (IMR), and IS were assessed 2 days after primary percutaneous coronary intervention and at the 5-month follow-up. The predictors of the 5-month IS were the baseline values of IS (beta=0.6, P<0.001), IMR (beta=0.280, P=0.013), and CFR (beta=-0.276, P=0.017). There were significant correlations between relative change in IS and relative change in measures of microvascular function (IS and CFR [r=-0.51, P=0.002]); IS and IMR ([r=0.55, P=0.001]). In multivariate model, relative changes in IMR (beta=0.552, P=0.001) and CFR (beta=-0.511, P=0.002) were the only predictors of relative change in IS. In patients with an improvement in IMR >33%, the mean IS decreased from 32.3+/-16.9% to 19.3+/-14% (P=0.001) in the follow-up. Similarly, in patients with an improvement in CFR >41%, the mean IS significantly decreased from 29.9+/-20% to 15.8+/-12.4% (P=0.003). But in patients with an improvement in IMR and CFR, which were below than the mean values, IS did not significantly decrease during the follow-up., Conclusions: Improvement in microvascular function in the infarcted territory is associated with reduction in IS after reperfused ST-elevation acute myocardial infarction. This link suggests that further investigations are warranted to determine whether therapeutic protection of microvascular integrity results in augmentation of infarct healing.

Background: After acute myocardial infarction (AMI), the recovery of perfusion in infarct area may lead to significant spontaneous infarct size (IS) reduction during the subsequent period. The natural course of infarct-healing process after reperfusion therapy has not been fully elucidated. In this study, we investigated the time course of the spontaneous infarct-healing process in patients with reperfused AMI., Methods and Results: Fifty-two patients with AMI who underwent primary percutaneous intervention were included. IS was measured with single-photon emission tomography using Bull's eye method at 4th day, at 5th, and at 10th months. IS was expressed as a percentage of the total myocardium. IS decreased by 33.6% at 5th month when compared with 4th day IS (from 26.3% +/- 18.8% to 17.5% +/- 12.9%, P < 0.001, n = 44). At 10th month, mean IS decreased by 21% when compared with 5th month IS (from 15.89% +/- 12.65% to 12.53% +/- 9.35%, P = 0.007, n = 31) and 49% when compared with 4th day IS (24.02% +/- 17.67% to 12.53% +/- 9.35%, P < 0.001)., Conclusion: Significant endogenous recovery of perfusion in the infarct area occurs at the long term in patients with reperfused AMI. Infarct healing is a dynamic and ongoing process and decrease in IS continues long term after reperfused AMI.

Objectives: The purpose of this study was to investigate the reflections of the improvement in microvascular perfusion provided by adjuvant intracoronary streptokinase (ICSK) on late-phase infarct size and left ventricular volumes and functions., Background: It has been shown that ICSK given immediately after primary percutaneous coronary intervention (PCI) improves myocardial perfusion in the early days of ST-segment elevation acute myocardial infarction., Methods: Ninety-five patients undergoing primary PCI were randomized to ICSK 250 kU (n = 51) or no additional therapy (n = 44). Two days later, coronary hemodynamic indexes were measured to evaluate tissue-level perfusion. After 6 months, angiography, echocardiography, and technetium-99m single-photon emission computed tomography (SPECT) were performed., Results: At 2 days, all indexes of microvascular function were significantly better in the ICSK group than in the control group, including coronary flow reserve (2.5 vs. 1.7, p < 0.001) and index of microvascular resistance (20.2 vs. 34.2, p < 0.001). At 6 months, infarct size (22.7% vs. 32.9%; p = 0.003) and left ventricular end-systolic (41.1 ml vs. 60.9 ml; p = 0.009) and end-diastolic volumes (95.5 ml vs. 118.3 ml; p = 0.006) were significantly smaller, and the ejection fraction was significantly higher (57.2% vs. 51.8%; p = 0.018) in the ICSK group compared with the control group., Conclusions: In this study, it has been demonstrated that low-dose ICSK given immediately after primary PCI significantly limits long-term infarct size and preserves left ventricular volumes and functions. (Effect of Complementary Intracoronary Streptokinase Administration Immediately After Primary Percutaneous Coronary Intervention on Microvascular Perfusion and Late Term Infarct Size in Patients With Acute Myocardial Infarction; NCT00302419).

Aim: The aim of the study was to determine if the tissue Doppler imaging (TDI)-derived myocardial acceleration during isovolumic contraction (IVA) of tricuspid lateral annulus could be used in early detection of RV systolic dysfunction in patients with mitral stenosis (MS), before the clinical signs of systemic venous congestion occur., Methods: One hundred and twelve patients with rheumatic MS without relevant regurgitation and 60 control subjects were enrolled in the study. Conventional echocardiographic parameters (mitral valve area, transmitral diastolic gradients, pulmonary artery pressure, RV fractional shortening, pulmonary flow acceleration time, tricuspid annular plane systolic excursion) and TDI-derived systolic velocities of tricuspid annulus (isovolumic myocardial acceleration: IVA, peak myocardial velocity during isovolumic contraction: IVV, peak systolic velocity during ejection period: Sa and RV Tei index) were recorded from all patients., Results: TDI-derived IVA, IVV, Sa and Tei index were found to be significantly decreased in patients with MS. IVA was the only parameter which had a significant negative correlation with the traditional echocardiographic parameters and RV Tei index in patients with MS. Additionally, in subgroup analyses, IVA was significantly lower in patients with severe degree of MS., Conclusion: TDI-derived right ventricular IVA may be used as an adjunctive, reliable, noninvasive parameter for the early detection of right ventricular systolic dysfunction in patients with MS but without signs of systemic venous congestion.

Pulmonary embolus sourced by right atrial thrombus trapped in a patent foramen ovale is an unusual, rare condition. Thus in suspicion of massive pulmonary thromboembolus, echocardiographic examination carries great importance evaluate right ventricular functions and diagnose right sided intracardiac thrombus. We report a 76-year-old female with massive pulmonary embolism caused by a gigantic thrombus trapped in a patent foramen ovale. The echocardiography was the diagnostic procedure to display the source of the thromboembolism and urgent cardiac surgery was successful and life-saving treatment in this case.