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Myocardial bridging (MB) is a congenital coronary anomaly in which a segment of the epicardial coronary artery traverses through the myocardium for a portion of its length. The muscle overlying the artery is termed a myocardial bridge, and the intramyocardial segment is referred to as a tunneled artery. MB can occur in any coronary artery, although is most commonly seen in the left anterior descending artery. Although traditionally considered benign in nature, increasing attention is being given to specific subsets of MB associated with ischemic symptomatology. The advent of contemporary functional and anatomic imaging modalities, both invasive and noninvasive, have dramatically improved our understanding of dynamic pathophysiology associated with MBs. This review provides a contemporary overview of epidemiology, pathobiology, diagnosis, functional assessment, and management of MBs.

Takotsubo syndrome (TS) is an acute and reversible form of myocardial stunning preceded by emotional or physical stress, not explained by an obstruction of an epicardial coronary artery as in acute coronary syndrome. Over the last decades, TS is receiving growing attention, leading to an increase in awareness and diagnostic rate. Chest pain and dyspnea are the most common presenting symptoms; however, nonspecific presentations make the diagnosis challenging for clinicians. Here, we present the case of a 76-year-old female who experienced two completely asymptomatic episodes of TS 20 years apart.

Objectives: Myocardial bridges (MB) are a congenital anomaly in which part of the epicardial coronary artery is intramuscular, known as the presence of myocardium, which causes narrowing of the artery during heart contraction. We aimed to evaluate hemogram parameters (especially platelet indices) in diabetic patients with myocardial bridges. Methods: We reviewed angiograms performed between May 2017 and August 2019 at Bolu Abant Izzet Baysal University Medical Faculty Hospital. After appropriate exclusions, diabetic patients were divided into groups with myocardial bridges and normal coronary artery groups. A total of 124 patients were included in the study and hemogram parameters of these two groups were compared. Kolmogorov Smirnov test was used to examine the normality of variables. Data were compared using univariate tests including independent samples t-test, Mann–Whitney U-test and chi-square test. Results: Compared to control group PDW (17.7 (15.9-19.5) vs.17.4 (16.2-18.9) % p=0.047), MPV (8.3 (6.6-11.4) vs. 7.5 (6.6-8.7) Fl p

Myocardial bridging (MB) is characterised by a segment of a major epicardial coronary artery tunnelling through the myocardium, which is a frequent congenital anomaly, detected in 15–85% of autopsy series and in 0.5–33% of angiographic studies.[1,2][1] MB without critical stenosis is generally

Purpose: Patients with angina and a positive SPECT for reversible ischemia, with no or non-obstructive CAD on ICA represent a frequent clinical problem and predicting prognosis is challenging. Methods: A retrospective single center study focused on patients that underwent elective-ICA with angina and a positive SECT with no or non-obstructive CAD in the CathLab, during a seven-year period. Assessment of patients’ cardiovascular morbidity, mortality, and MACE during a follow-up period of at least three years after ICA, with the assist of a telephone questionnaire.Results: Data of all patients that underwent ICA for a period of 7 years (from January 1,2011 until December 31, 2017) in our hospital were analyzed. The patients that fulfilled the prespecified criteria were 569. At the telephone survey, 285(50.1%) were successfully contacted and agreed to participate. The mean age was 67.6 (SD8.8) years (35.4%female) and the mean follow-up time was 5.53years (SD1.85). Mortality rate was 1.7% (4 patients/non-cardiac causes) and 1,7% rate of revascularization. 31(10,9%) were hospitalized for cardiac reasons and 10,9% patients reported symptoms of HF (no patients with NYHA-Class above II). 21 had arrhythmic events and only two mild anginal symptoms. Noteworthy finding was, the mortality rate in the not-contacted group (12 out of 284, 4,2%), derived by public security records, did not differ significantly from the contacted-group. Conclusions: Patients with angina, a positive SPECT for reversible ischemia and no or non-obstructive CAD in ICA have very good long-term cardiovascular prognosis for at least 5 years.

The goal of reperfusion therapies in ST-segment elevation myocardial infarction has evolved to include effective reperfusion of the microcirculation subtended by the culprit epicardial coronary artery. The index of microcirculatory resistance is measured using a pressure- and temperature-sensing coronary guidewire and quantifies microvascular dysfunction. The index of microcirculatory resistance is an independent predictor of microvascular obstruction, infarct size, and adverse clinical outcomes. It has the advantage of being immediately measurable in the catheterization laboratory, before the results of blood biomarkers or noninvasive imaging become available. This provides an opportunity for additional intervention that may alter outcomes. In this review, the authors provide a critical appraisal of the published research on the emerging role of the index of microcirculatory resistance as a tool to guide the stratification of patients for adjunctive therapeutic strategies in acute ST-segment elevation myocardial infarction.

Recent studies reported at TCT Connect 2020 have investigated a number of open clinical questions regarding the role of coronary physiology and the assessment of plaque morphology for diagnosis (FORECAST), risk stratification (COMBINE OCT-FFR) and treatment evaluation (DEFINE-PCI) of patients with coronary artery disease. In this article, the authors provide a critical appraisal of these studies and evaluate how they add to the current evidence base for management of patients with epicardial coronary artery disease. Furthermore, they discuss their potential impact on clinical practice, limitations of these studies and unanswered clinical questions that are areas for future research.

Background Coronary artery spasm is an established cause for angina pectoris. Epicardial coronary spasm may occur in patients with obstructed as well as unobstructed coronary arteries. Previous studies have suggested that epicardial plaque/atherosclerosis is a prerequisite for the development of epicardial spasm. The aim of the present study was to compare the results of intracoronary acetylcholine (ACh) testing in patients with signs and symptoms of myocardial ischemia with completely smooth versus atherosclerotic yet unobstructed epicardial arteries. Methods Between 2008 and 2016 a total number of 617 patients with signs and symptoms of myocardial ischemia yet unobstructed epicardial arteries ( Results There were 389 patients (63%) with completely smooth epicardial arteries. The remaining 228 patients (37%) had non-obstructive epicardial plaques Conclusion In patients with signs and symptoms of myocardial ischemia yet unobstructed coronary arteries the presence of epicardial atherosclerosis is an independent predictor for the occurrence of epicardial spasm but not microvascular spasm on acetylcholine testing. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): Robert-Bosch-Stiftung, Berthold-Leibinger-Stiftung

Background Coronary functional abnormalities including both epicardial and microvascular coronary artery spasm represent an important role responsible for myocardial ischemia in patients with angina and nonobstructive coronary artery disease. However, clinical characteristics associated with microvascular spasm (MVS) have not been fully evaluated. Purpose The aim of this study was to assess differences in clinical features between patients with MVS and epicardial coronary spasm. Methods A total of 732 consecutive patients with suspected angina who presented nonobstructive coronary arteries and underwent intracoronary acetylcholine provocation test were retrospectively enrolled in this study. Epicardial coronary spasm was defined as total or subtotal occlusion of epicardial coronary arteries accompanied by chest pain and/or ischemic electrocardiographic changes in response to acetylcholine provocation test. MVS was diagnosed when chest pain and/or ischemic electrocardiographic changes developed after administration of acetylcholine in the absence of epicardial coronary spasm. Clinical characteristics were compared between patients with MVS and epicardial coronary spasm. Results Of all patients, 83 patients (11%) had MVS, 367 (50%) had epicardial coronary spasm, and the other patients (39%) showed neither MVS nor epicardial coronary spasm. Patients with MVS tended to be older (65.6±12.7 vs. 63.0±12.3 years, P=0.088) and were more frequently female (60.2% vs. 41.1%, P=0.0016) in comparison with patients with epicardial coronary spasm. Patients with MVS were less likely to be smokers (8.6% vs. 22.9%, P=0.0018), while there were no significant differences in the other coronary risk factors such as hypertension, dyslipidemia, and diabetes mellitus. Serum uric acid were significantly lower in patients with MVS (4.9±1.1 vs. 5.4±1.3 mg/dl, P=0.0018). Conclusion Our study demonstrated that patients with MVS had distinctive clinical background from those with epicardial coronary spasm, suggesting different mechanisms may involve the development of MVS. Funding Acknowledgement Type of funding source: None

Supplemental Digital Content is available in the text., Background: Spontaneous coronary artery dissection (SCAD) occurs when an epicardial coronary artery is narrowed or occluded by an intramural hematoma. SCAD mainly affects women and is associated with pregnancy and systemic arteriopathies, particularly fibromuscular dysplasia. Variants in several genes, such as those causing connective tissue disorders, have been implicated; however, the genetic architecture is poorly understood. Here, we aim to better understand the diagnostic yield of rare variant genetic testing among a cohort of SCAD survivors and to identify genes or gene sets that have a significant enrichment of rare variants. Methods: We sequenced a cohort of 384 SCAD survivors from the United Kingdom, alongside 13 722 UK Biobank controls and a validation cohort of 92 SCAD survivors. We performed a research diagnostic screen for pathogenic variants and exome-wide and gene-set rare variant collapsing analyses. Results: The majority of patients within both cohorts are female, 29% of the study cohort and 14% validation cohort have a remote arteriopathy. Four cases across the 2 cohorts had a diagnosed connective tissue disorder. We identified pathogenic or likely pathogenic variants in 7 genes (PKD1, COL3A1, SMAD3, TGFB2, LOX, MYLK, and YY1AP1) in 14/384 cases in the study cohort and in 1/92 cases in the validation cohort. In our rare variant collapsing analysis, PKD1 was the highest-ranked gene, and several functionally plausible genes were enriched for rare variants, although no gene achieved study-wide statistical significance. Gene-set enrichment analysis suggested a role for additional genes involved in renal function. Conclusions: By studying the largest sequenced cohort of SCAD survivors, we demonstrate that, based on current knowledge, only a small proportion have a pathogenic variant that could explain their disease. Our findings strengthen the overlap between SCAD and renal and connective tissue disorders, and we highlight several new genes for future validation.

This article offers an updated and comprehensive overview of major findings on the effects of statin treatment in patients with chronic angina but without any epicardial coronary artery with obstructive lesion.

When epicardial arteries with minimal CAD do not limit flow are found at coronary angiography, all cardiologists agree that aggressive risk factor modification and use of appropriate drugs are warranted. Some consider plaque sealing of minor coronary lesions with balloon angioplasty to prevent future infarction. Others believe that a coronary lesion that does not cause ischemia should not have the plaque sealed but should have FFR and the non-ischemia producing stenosis should be treated with aggressive risk factor modification (DEFER study). Evidence based data e.g. DEFER, relates to populations, not the individual. Thus these data provide guidelines, which are suggestions for decision making. The weight of evidence favors angioplasty/stent for epicardial vessels that result in myocardial ischemia. Sealing of non flow limiting plaques with angioplasty must await further information derived from invasive and non invasive studies.

Coronary vasospasm is characterized by focal or diffuse spasm of an epicardial coronary artery. Definitive diagnosis is usually made with coronary angiography, when resolution of stenosis is observed after administration of intracoronary vasodilators. Coronary vasospasm is rarely a consequence of a blunt force injury to the chest. Among trauma induced cardiac complications, coronary vasospasm has been the least common with only one other reported case of coronary vasospasm induced by trauma. We report a rare case of severe spontaneous coronary vasospasm in a patient with polytrauma successfully treated with intracoronary, intravenous and oral vasodilator therapy. The mechanism is thought to be due to compensatory catecholamine response to trauma, and coronary vasospasm should be strongly suspected in trauma patients with unexplained hypotension, new conduction abnormalities or evidence of ischemia on the ECG. Keywords: Coronary vasospasm, Vasospastic angina, Angina pectoris, Atherosclerotic disease, Polytrauma

To investigate the association between serum C-reactive protein (CRP) levels and coronary collateral circulation (CCC) in Chinese patients with angiography-proven ≥95% coronary stenosis.In this study, 1158 patients with angiography-proven ≥95% occlusion in ≥1 major epicardial coronary artery were enrolled, and then classified into two groups: poor CCC (Rentrop grades 0-1) and good CCC (Rentrop grades 2-3). CRP levels were grouped using the following two models: Model 1 discretized CRP group with 33.33% and 66.66% as the critical values and Model 2 with 1.0 and 3.0 mg/L as the cut off values.There were significant differences in serum CRP levels between the two groups (5.76 ± 3.45 vs. 3.49 ± 2.44 mg/L, respectively; p 0.001), and compared with the first CRP tertile, the risks of poor CCC were higher in the second and third CRP tertiles (OR 2.31, 95%CI [1.67-3.19], OR 6.25, 95%CI [4.52-8.62], respectively). The receiver operating characteristic curve analysis indicated that the optimal cutoff value of CRP to predict poor CCC was 4.21 mg/L with 59.6% sensitivity and 74.33% specificity.CRP levels are an independent predictor for poor CCC and might supply a useful biomarker in clinical applications. Key messages C-reactive protein (CRP) is a non-specific inflammatory marker that is regarded as an independent risk and prognostic factor for individuals who suffer from coronary artery disease (CAD) and cardiovascular disorders. In a Chinese cohort of patients with coronary artery occlusion or stenosis of ≥95% TIMI grade 1 anterograde-flow, the relationship between CRP concentrations and angiographically visible coronary collateral (CC) was assessed. Our data indicated that elevated CRP associated with a significant impairment in CC development, and might supply a useful biomarker in clinical applications.

A myocardial bridge is a segment of an epicardial coronary artery tunneled within the myocardium, which clinically ranges from an incidental finding to an etiology of acute coronary syndrome. Determining the hemodynamic significance with instantaneous wave-free ratio (iFR) can guide medical vs.

Background: Band of Myocardial tissue overlying a segment of an epicardial coronary artery is termed myocardial bridge (MB). The aim of this study was to identify the prevalence, risk factors and angiographic profile of patients with myocardial bridge in a tertiary care hospital, Dhaka, Bangladesh. Materials and Methods: This retrospective observational study included a total of 1480 patients with suspected coronary artery disease admitted to Enam Medical College and Hospital, Savar, Dhaka, Bangladesh for coronary angiography between April 2016 to June 20019 of them 43 cases were found to have myocardial bridge. Coronary compression was defined as a maximum systolic luminal compression ≥50%. In this population, 43 patients had systolic luminal compression ≥50%, and all 43 patients were selected for the study to determine the prevalence and risk factors of MB and recorded coronary angiogram was reviewed to see the angiographic location of MB, length of MB and number of vessels involved. Results: In this study incidence of MB was 2.9%. The risk factors associated with MB hypertension were 33 (76.74%), diabetes mellitus 28 (65.11%), hyperlipidaemia 18 (41.86%), family history of CAD 15 (34.88%), smoking history 22 (51.16%). Located of MB in LAD were 34 (79.06%), LCX 07 (16.27%) and RCA 02 (4.65%). The MB were in single vessel 38 (88.37%) and double vessels 05 (11.62%). MBs with atherosclerotic stenosis in LAD were 18 (41.86%), LCX 02 (4.65%), RCA 01 (2.32%) and severity of MB stenosis were in LAD 50 -70% were 27 (62.79%), >70% were 07 (16.27%), LCX 50-70% were 06 (13.95%) and >70% was 01 (2.32%) and RCA 50-70% was 02 (4.65%). The length of MBs segment 20 mm were 12 (27.90%). Conclusion: In this study the prevalence of MB was 2.91%, commonly presented with chronic stable angina. The most risk factors of myocardial bridges were hypertension, diabetes mellitus, hyperlipidaemia, family history and smoking history. In coronary angiography most of the patient of MB was present in association of acute coronary syndrome with documented coronary artery disease and was mainly located in LAD mid segment and the length of MB was mostly 10-20 mm. Further large numbers of case are needed to validate the result of the study.

It remains unclear if the human coronary vasculature is inherently sensitive to changes in arterial Po2 and Pco2 or if coronary vascular responses are the result of concomitant increases in myocardial O2 consumption/demand ([Formula: see text]). We hypothesized that the coronary vascular response to Po2 and Pco2 would be attenuated in healthy men when [Formula: see text] was attenuated with β1-adrenergic receptor blockade. Healthy men (age: 25 ± 1 yr, n = 11) received intravenous esmolol (β1-adrenergic receptor antagonist) or volume-matched saline in a double-blind, randomized crossover study and were exposed to poikilocapnic hypoxia, isocapnic hypoxia, and hypercapnic hypoxia. Measurements made at baseline and after 5 min of steady state at each gas manipulation included left anterior descending coronary blood velocity (LADV; Doppler echocardiography), heart rate, and arterial blood pressure. LADV values at the end of each hypoxic condition were compared between esmolol and placebo. The rate-pressure product (RPP) and left ventricular mechanical energy (MELV) were calculated as indexes of [Formula: see text]. All gas manipulations augmented RPP, MELV, and LADV, but only RPP and MELV were attenuated (4–18%) after β1-adrenergic receptor blockade ( P < 0.05). Despite attenuated RPP and MELV responses, β1-adrenergic receptor blockade did not attenuate the mean LADV vasodilatory response compared with placebo during poikilocapnic hypoxia (29.4 ± 2.2 vs. 27.3 ± 1.6 cm/s) and isocapnic hypoxia (29.5 ± 1.5 vs. 30.3 ± 2.2 cm/s). Hypercapnic hypoxia elicited a feedforward coronary dilation that was blocked by β1-adrenergic receptor blockade. These results indicate a direct influence of arterial Po2 on coronary vascular regulation that is independent of [Formula: see text]. NEW & NOTEWORTHY In humans, arterial hypoxemia led to an increase in epicardial coronary artery blood velocity. β1-Adrenergic receptor blockade did not diminish the hypoxemic coronary response despite reduced myocardial O2 demand. These data indicate hypoxemia can regulate coronary blood flow independent of myocardial O2 consumption. A plateau in the mean left anterior descending coronary artery blood velocity-rate-pressure product relationship suggested β1-adrenergic receptor-mediated, feedforward epicardial coronary artery dilation. In addition, we observed a synergistic effect of Po2 and Pco2 during hypercapnic hypoxia.

Background: It is important to determine the grade of the coronary collateral circulation (CCC) in patients with stable coronary artery disease. Aim: In this study, we aimed to investigate the relationship between the ischaemia-modified albumin (IMA) level and good CCC. Methods: A total of 95 patients with coronary angiography and at least one epicardial coronary artery obstruction were included in the study. The Rentrop classification was used with CCC grading, where 0 and 1 were defined as poor collateral, and 2 and 3 were defined as good collateral. The IMA level of the patients was measured using an enzyme-linked immunosorbent assay (ELISA). The receiver–operating characteristic curve was used to show the sensitivity and specificity of IMA levels and the optimal cut-off value for predicting good CCC. Results: The multiple logistic regression analysis revealed that the IMA level in the good CCC group was higher (p < 0.045). Conversely, the high-sensitivity C-reactive protein level was lower in the good CCC group (p < 0.023). We found an IMA cut-off value (4.7 ng/mL) that indicated good CCC level, and this shows good CCC with 70.2% sensitivity and 60.3% specificity. Conclusions: The IMA level could serve as a simple and useful predictor of well-developed CCC.

The times, they are a-changin’. —Bob Dylan [(1)][1] Almost 20 years ago, fractional flow reserve (FFR) assessment performed at the time of invasive coronary angiography (ICA) was introduced as a method for identifying and excluding stenoses that reduced epicardial coronary artery flow [(2)][2

Fractional flow reserve (FFR) is the gold standard in the invasive hemodynamic assessment of epicardial coronary artery stenoses. FFR is defined as the ratio of maximal flow achievable in the stenotic coronary artery to the maximal flow achievable in the same coronary artery if it was normal. In other words, FFR informs the clinician to what extent blood flow is reduced and can be improved after revascularization: e.g., a FFR of 0.60 means that coronary blood flow is 60% of what should be in the absence of the epicardial stenosis, and it could improve by 40% after percutaneous coronary intervention.

Rapid and sustained restoration of antegrade flow through the epicardial coronary artery is the primary goal of current treatment of acute ST-segment elevation myocardial infarction (STEMI). It consists of a combination of mechanical recanalization of the occluded artery with primary percutaneous

Myocardial bridging (MB) is characterized by epicardial coronary artery tunneling through the myocardium, with angiographic “milking” and an intravascular ultrasound (IVUS) “half-moon” echolucent [(1)][1]. Optical coherence tomography (OCT), a light-based technique, can provide unprecedented

We present cardiac computed tomography (CT) findings demonstrating apical hypertrophic cardiomyopathy with dystrophic calcification of the left ventricular apex. The absence of significant epicardial coronary artery disease demonstrated by coronary CT angiography suggests that increased wall tension and decreased microvascular perfusion over time account for the dyskinetic apical myocardium, rather than myocardial infarction secondary to atherosclerotic plaque rupture. These observations support CT as the imaging modality of choice to visualize the deposition of calcium in injured myocardial tissue, a recognized occurrence in chronically infarcted myocardium.

An under-recognized cause of chest pain and acute coronary syndromes, the coronary slow flow (CSF) phenomenon is characterized by delayed coronary opacification during diagnostic angiography in the absence of epicardial coronary artery disease or other conditions known to impair coronary flow.

Myocardial bridging (MB) is a congenital anomaly in which a segment of an epicardial coronary artery takes a tunneled intramuscular course under overlying myocardium. Rarely, MB can cause ST elevation myocardial infarction (STEMI). 39 year old male patient presented with 24 hours of typical chest

Race is a component of the Atherosclerotic Cardiovascular Disease (ASCVD) risk score. How ASCVD risk relates to cardiac events and epicardial coronary artery disease (CAD) in blacks vs whites with stable chest pain is not known. The PROMISE trial included 8,764 non-Hispanic blacks (12%; 1,071) and

Slow coronary flow (SCF) phenomenon is a coronary microvascular disorder characterized by the delayed passage of angiographic contrast in the absence of obstructive epicardial coronary artery disease (CAD). Many patients with SCF suffer from angina-like chest pain and present for angiography

Intracoronary acetylcholine provocation testing (ACH-test) is an established method for assessment of epicardial coronary artery spasm in the catheterization laboratory which was introduced more than 30 years ago. Due to the short half-life of acetylcholine it can only be applied directly into the coronary arteries. Several studies have demonstrated the safety and clinical usefulness of this test. However, acetylcholine testing is only rarely applied in the U.S. or Europe. Nevertheless, it has been shown that 62% of Caucasian patients with stable angina and unobstructed coronary arteries on coronary angiography suffer from coronary vasomotor disorders that can be diagnosed with acetylcholine testing. In recent years it has been appreciated that the ACH-test not only assesses the presence of epicardial spasm but that it can also be useful for the detection of coronary microvascular spam. In such cases no epicardial spasm is seen after injection of acetylcholine but ischemic ECG shifts are present together with a reproduction of the patient's symptoms during the test. This article describes the experience with the ACH-test and its implementation in daily clinical routine.

Takotsubo cardiomyopathy is characterized by transient systolic ballooning of apical or mid segments of the left ventricle (LV) mimicking acute myocardial infarction in the absence of obstructive epicardial coronary artery disease. Recurrences remain rare and most recurrence case reports are about apical ballooning or typical Takotsubo cardiomyopathy. We present a rare case of recurrence in mid ventricular ballooning or atypical variant of Takotsubo cardiomyopathy. This case highlights the importance of future follow-up and potential of recurrence even in atypical variants.

Background: Treadmill exercise testing has low specificity for the detection of significant epicardial coronary artery disease (CAD). A possible mechanism to explain some of the false positives is transient subendocardial ischemia induced by intraventricular gradients (IVG) during stress. The development of IVG during dobutamine stress echocardiography (DSE) occurs in 8-38% of non-selected populations. Objectives: To determine: 1. the prevalence of IVG in a selected population of false positives on treadmill stress testing; 2. whether this prevalence is different from that described for non-selected populations; 3. whether patient characteristics are related to the presence of IVG; 4. the relation between the presence of IVG and the occurrence of ECG abnormalities, symptoms and blood pressure. Methods and Results: We evaluated 50 consecutive patients with false positive treadmill stress tests (normal CT coronary angiography, nuclear perfusion tests or angiography) with DSE (2D and Doppler evaluation). All DSE exams were negative for ischemia. Stress-induced IVG was seen in 34 of the 50 patients (68%) and 16 patients (32%) did not develop IVG (p 0.05). However, the presence of IVG was associated with the occurrence of ischemic ST depression during dobutamine stress echo (p 0,05). No entanto, a presença de GIV relacionou-se com a ocorrência de depressão do segmento ST durante o ecocardiograma de sobrecarga com dobutamina (p < 0,05). Conclusões: 1. A prevalência de GIV durante o ecocardiograma de stress com dobutamina em populações seleccionadas de falsos positivos de prova de esforço é muito elevada, ocorrendo em 2/3 dos doentes. 2. Esta prevalência é significativamente mais alta que a descrita para populações não seleccionadas. 3. Idade, género, factores de risco para DAC, terapêutica com beta-bloqueantes/antagonistas dos canais de cálcio, doença arterial significativa/HVE, sintomas e a pressão arterial durante a sobrecarga não se relacionam com a presença ou ausência de GIV. 4. A presença de GIV está relacionada com a ocorrência de alterações isquémicas do segmento ST durante a ecocardiografia de sobrecarga com dobutamina. Keywords: Treadmill stress tests, False positives, Stress echocardiography, Physical exercise, Intraventricular gradient, Palavras-chave: Prova de esforço, Falsos positivos, Ecocardiografia de sobrecarga, Exercício físico, Gradiente intraventricular

Coronary microvascular dysfunction (CMVD) can mediate angina and myocardial ischemia in a proportion of patients presenting with signs and symptoms of myocardial ischemia in the absence of obstructive epicardial coronary artery disease (CAD). Previous studies have shown sex based difference in

Fractional flow reserve (FFR) has become the reference standard for assessing the functional significance of epicardial coronary artery disease in the cardiac catheterization laboratory. Recently an alternative microcatheter derived fractional flow reserve (FFRMC) system has been developed. However

Fractional flow reserve (FFR) is a useful index for determining the functional severity of epicardial coronary artery stenosis as an invasive physiological method. Although intravenous adenosine 5'-triphosphate (ATP) is generally used as a hyperemic agent for FFR measurement in Japan, there are some concerns about the variability of FFR measurement (short half-life, effect of caffeine, cyclic change). It is difficult to confirm sufficient maximum hyperemia after ATP infusion. Recent studies reported that nicorandil (NIC) could be an alternative to ATP as a hyperemic agent.Patients who underwent FFR assessments of angiographically intermediate lesions were included. All patients were asked to refrain from caffeine-containing products more than 12hours before FFR measurements. All patients first received intravenous (IV) ATP infusion (180μg/kg/min) for 3min to measure FFR (ATP-FFR). After additional intracoronary (IC) NIC administration (2mg/30s) during ATP infusion, FFR was measured again (NIC-FFR). To check cyclic change in FFR, we measured minimum and maximum FFR values during both ATP and NIC hyperemic phase.In this study, 94 patients with 94 lesions were enrolled. Mean FFR value was 0.81±0.10 in ATP-FFR infusion and 0.80±0.09 in NIC-FFR, respectively. ATP-FFR and NIC-FFR had a strong correlation on the whole (r=0.92, p0.001). In 18 patients (19%), FFR values were significantly lower in NIC-FFR than in ATP-FFR. In one-third of those patients (6%), it was possible to change therapeutic strategy from deferral range (0.80) to interventional range (≦0.80) after NIC-FFR measurements. Cyclic change in FFR was smaller in NIC-FFR than in ATP-FFR (0.03±0.02 vs. 0.06±0.05, p0.0001).Additional IC NIC might be useful to confirm sufficient maximum hyperemia after IV ATP infusion in daily clinical practice. Furthermore, IC NIC could reduce cyclic change in FFR; thus, physicians might find it easier to determine FFR value during the procedure.

myocardial infarction (MI) is a leading cause of death and disability globally that typically results from the abrupt occlusion of an epicardial coronary artery ([9][1]). As a result, cardiomyocytes distal to the occlusion are subject to oxygen and nutrient deprivation, which triggers mitochondrial

Physicians cannot rely solely on the angiographic appearance of epicardial coronary artery stenosis when evaluating patients with myocardial ischemia. Instead, sound knowledge of coronary vascular physiology and of the methods currently available for its characterization can improve the diagnostic and prognostic accuracy of invasive assessment of the coronary circulation, and help improve clinical decision-making. In this article we summarize the current methods available for a thorough assessment of coronary physiology.

Prinzmetal variant angina due to epicardial coronary artery spasm is a disease usually treated with drug therapy with successful results. However, a small percentage of patients are resistant to medical therapy. In this report, we present a patient with recurrent vasospastic episodes who was refractory to conventional pharmacological treatment and successfully treated with an amiodarone treatment. We also discuss the therapeutic effectiveness of amiodarone therapy for vasospastic angina.

We describe a new variant of transient left ventricular (LV) ballooning in North American Caucasian patients in which only the midventricle is affected. The patients described in this case series initially presented with emotional or physical stress and had similarities to transient apical ballooning syndrome; however, this variant is unique in that the transient ballooning involves the midventricle with hypercontractility of the apical and basal segments. The presentation, clinical features, and transient nature of the reported cases in this series are similar to transient LV apical ballooning and suggest a shared pathophysiologic etiology. Sparing of the apical segment with involvement of midventricle only supports etiologies not related to an epicardial coronary artery distribution. Although the pathophysiologic mechanism of the transient ventricular ballooning syndromes and other cases of catecholamine-associated transient ventricular dysfunction are not well understood, the emergence of this new variant raises further questions in the understanding of the “brain-heart” relationship.

The index of microcirculatory resistance (IMR) is an invasive measure of the coronary microvascular function. To date, little is known about the collinearity in disease progression between microvascular and epicardial coronary artery. This study consisted of 93 patients who underwent three-vessel

Coronary artery spasm (CAS) refers to an abnormal condition where the epicardial coronary artery contracts. The relationship between alcohol consumption and CAS is even more ambiguous. Therefore, we evaluated drinking patterns such as current drinking status, weekly drinking amount, and drinking

Patients with angina and coronary microvascular dysfunction (CMVD) in the absence of obstructive epicardial coronary artery disease (CAD) or structural heart disease (Type 1 CMVD) remain without evidence based treatment options. Ranolazine has been shown to reduce frequency of angina episodes among