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Cardioplegic ischemia–reperfusion and diabetes mellitus are correlated with coronary endothelial dysfunction and inactivation of small conductance calcium-activated potassium channels. Increased reactive oxidative species, such as mitochondrial reactive oxidative species, may contribute to oxidative injury. Thus, we hypothesized that inhibition of mitochondrial reactive oxidative species may protect coronary small conductance calcium-activated potassium channels and endothelial function against cardioplegic ischemia–reperfusion-induced injury. Small coronary arteries and endothelial cells from the hearts of mice with and without diabetes mellitus were isolated and examined by using a cardioplegic hypoxia and reoxygenation model to determine whether the mitochondria-targeted antioxidant Mito-Tempo could protect against coronary endothelial and small conductance calcium-activated potassium channel dysfunction. The microvessels or mouse heart endothelial cells were treated with or without Mito-Tempo (0-10 μM) 5 minutes before and during cardioplegic hypoxia and reoxygenation. Microvascular function was assessed in vitro by vessel myography. K+ currents of mouse heart endothelial cells were measured by whole-cell patch clamp. The levels of intracellular cytosolic free calcium (Ca2+) concentration, mitochondrial reactive oxidative species, and small conductance calcium-activated potassium protein expression of mouse heart endothelial cells were measured by Rhod-2 fluorescence staining, MitoSox, and Western blotting, respectively. Cardioplegic hypoxia and reoxygenation significantly attenuated endothelial small conductance calcium-activated potassium channel activity, caused calcium overload, and increased mitochondrial reactive oxidative species of mouse heart endothelial cells in both the nondiabetic and diabetes mellitus groups. In addition, treating mouse heart endothelial cells with Mito-Tempo (10 μM) reduced cardioplegic hypoxia and reoxygenation-induced Ca2+ and mitochondrial reactive oxidative species overload in both the nondiabetic and diabetes mellitus groups, respectively (P <. 05). Treatment with Mito-Tempo (10 μM) significantly enhanced coronary relaxation responses to adenosine 5′-diphosphate and NS309 (P <. 05), and endothelial small conductance calcium-activated potassium channel currents in both the nondiabetic and diabetes mellitus groups (P <. 05). Administration of Mito-Tempo improves endothelial function and small conductance calcium-activated potassium channel activity, which may contribute to its enhancement of endothelium-dependent vasorelaxation after cardioplegic hypoxia and reoxygenation. MT-induced endothelial protection in the setting of CP hypoxia and DM. [Display omitted] [ABSTRACT FROM AUTHOR]

• Modified coronary flow capacity (mCFC) by positron emission tomography is based on myocardial perfusion. • mCFC may reflect microvascular dysfunction in coronary artery disease (CAD). • Impaired mCFC was associated with both cardiovascular death and combined events. • mCFC may help identify CAD-suspected patients who benefit from specific therapies. Vasodilator capacity of coronary circulation is an important diagnostic and prognostic tool in patients with coronary artery disease (CAD). We aimed to clarify the incidence of coronary microvascular dysfunction (CMD), defined as impaired modified coronary flow capacity (mCFC) proposed by Johnson and Gould and measured by 13N-ammonia myocardial perfusion positron emission tomography (PET), in patients without obstructive CAD and to evaluate the risk of future cardiovascular events. This retrospective study recruited 407 consecutive CAD-suspected patients who underwent both pharmacological stress/rest 13N-ammonia PET and coronary angiography. Of the 407 patients, 137 patients (median age, 70 years; 63 women) were eligible and followed up (median, 19.8 months). Endpoints were defined as cardiovascular death or major adverse cardiovascular events (MACEs), such as cardiovascular death, nonfatal myocardial infarction, unplanned hospitalization for any cardiac reasons, and unplanned coronary revascularization. The impaired mCFC group included patients with mildly to severely reduced regional CFC in, at least, one vascular territory (n=34), while the remaining patients (n=103) were categorized as having preserved mCFC. Overall, cardiovascular death and MACEs occurred in five (4%) patients. The Kaplan–Meier curve showed a significant reduction in event-free survival for cardiovascular death (p =0.004) and MACEs (p <0.0001) in the impaired mCFC group, compared to the preserved mCFC group. Impaired mCFC was independently associated with the incidence of both cardiovascular death and MACEs after propensity-score adjustments [hazard ratio (HR), 10.7; 95% confidence interval (CI), 1.0–106.0; p =0.04 and HR, 9.5; 95% CI, 2.5–36.2; p <0.001, respectively]. In CAD-suspected patients without obstructive coronary arteries, impaired mCFC was observed in approximately 25% and was associated with a higher risk of cardiovascular death and MACEs. The mCFC concept can help identify patients who would benefit from specific therapies or lifestyle modifications to prevent future MACEs and can clarify potential mechanisms of CMD. [Display omitted] [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the diagnostic accuracy and prognostic implications of angiography-derived index of microcirculatory resistance (angio-IMR) in patients with ST-segment elevation myocardial infarction (STEMI). The index of microcirculatory resistance (IMR) is a reliable invasive measure of coronary microvascular dysfunction in patients with STEMI. A functional coronary angiography–derived method to estimate IMR is a wire- and hyperemic agent–free alternative to IMR. The study population consisted of 2 independent cohorts. The diagnostic cohort comprised patients with IMR from the culprit vessel immediately after successful primary percutaneous coronary intervention (n = 31). The prognostic cohort was patients with STEMI who were successfully treated with primary percutaneous coronary intervention and followed for 10 years from the index procedure (n = 309). Angio-IMR was calculated using computational flow and pressure simulation. The primary outcome was a composite of cardiac death and readmission for heart failure over 10 years of follow-up. In the diagnostic cohort, angio-IMR correlated well with IMR (R = 0.778; P < 0.001). Sensitivity, specificity, accuracy, and area under the curve of angio-IMR to predict IMR >40 U were 75.0%, 84.2%, 80.6%, and 0.899 (95% confidence interval: 0.786-0.949), respectively. In the prognostic cohort, patients with angio-IMR >40 U showed significantly higher risk for cardiac death or readmission for heart failure than did those with angio-IMR ≤40 U (46.7% vs 16.6%; adjusted hazard ratio: 2.909; 95% CI: 1.670-5.067; P < 0.001). Angio-IMR >40 U was an independent predictor of cardiac death or readmission for heart failure (hazard ratio: 2.173; 95% CI: 1.157-4.079; P = 0.016) and showed incremental prognostic value compared with a model with clinical risk factors only (C index = 0.726 vs 0.666 [ P < 0.001], net reclassification index = 0.704 [ P < 0.001]). Angio-IMR showed high correlation and diagnostic accuracy to predict IMR. Patients with STEMI with angio-IMR >40 U showed a significantly higher risk for cardiac death or readmission for heart failure than those with preserved angio-IMR values. (Prognostic Implication of Angiography-Derived IMR in STEMI Patients; NCT04628377) [Display omitted] [ABSTRACT FROM AUTHOR]

To investigate coronary endothelial protection of a small-conductance calcium-activated potassium (SK) channel activator against a period of cardioplegic-hypoxia and reoxygenation (CP-H/R) injury in mice and patients with diabetes (DM) and those without diabetes (nondiabetic [ND]). Mouse small coronary arteries/heart endothelial cells (MHECs) and human coronary arterial endothelial cells (HCAECs) were dissected from the harvested hearts of mice (n = 16/group) and from discarded right atrial tissue samples of patients with DM and without DM (n = 8/group). The SK current density of MHECs was measured. The in vitro small arteries/arterioles, MHECs, and HCAECs were subjected to 60 minutes of CP hypoxia, followed by 60 minutes of oxygenation. Vessels were treated with or without the selective SK activator NS309 for 5 minutes before and during CP hypoxia. DM and/or CP-H/R significantly inhibited the total SK currents of MHECs and HCAECs and significantly diminished the mouse coronary relaxation response to NS309. Administration of NS309 immediately before and during CP hypoxia significantly improved the recovery of coronary endothelial function, as demonstrated by increased relaxation responses to adenosine 5′-diphosphate and substance P compared with those seen in controls (P <.05). This protective effect was more pronounced in vessels from ND mice and patients compared with DM mice and patients (P <.05). Cell surface membrane SK3 expression was significantly reduced after hypoxia, whereas cytosolic SK3 expression was greater than that of the sham control group (P <.05). Application of NS309 immediately before and during CP hypoxia protects mouse and human coronary microvasculature against CP-H/R injury, but this effect is diminished in the diabetic coronary microvasculature. SK inhibition/inactivation and/or internalization/redistribution may contribute to CP-H/R–induced coronary endothelial and vascular relaxation dysfunction. NS309 activates SK channels, leading to endothelial protection/coronary relaxation. [ABSTRACT FROM AUTHOR]

Microcirculation is a system composed of interconnected microvessels, which is responsible for the distribution of oxygenated blood among and within organs according to regional metabolic demand. Critical medical conditions, e. g., sepsis, and heart failure are known triggers of microcirculatory disturbance, which usually develops early in such clinical pictures and represents an independent risk factor for mortality. Therefore, hemodynamic resuscitation aiming at restoring microcirculatory perfusion is of paramount importance. Until recently, however, resuscitation protocols were based on macrohemodynamic variables, which increases the risk of under or over resuscitation. The introduction of hand-held video-microscopy (HVM) into clinical practice has allowed real-time analysis of microcirculatory variables at the bedside and, hence, favored a more individualized approach. In the cardiac intensive care unit scenario, HVM provides essential information on patients' hemodynamic status, e. g., to classify the type of shock, to adequate the dosage of vasopressors or inotropes according to demand and define safer limits, to guide fluid therapy and red blood cell transfusion, to evaluate response to treatment, among others. Nevertheless, several drawbacks have to be addressed before HVM becomes a standard of care. [ABSTRACT FROM AUTHOR]

Objectives The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries. Background An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters. Methods Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11). Results In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = −0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p < 0.001) with consistent observations in swine (Δ = −0.9; 1.5 ± 0.4 vs. 2.4 ± 0.9 for after and before AMI, respectively; p = 0.04). An increased baseline and a decreased hyperemic flow contributed to the reduction in CFR in both patients (baseline flow: Δ = +5 and hyperemic flow: Δ = −7 cm/s) and swine (baseline flow: Δ = +8 and hyperemic flow: Δ = −6 cm/s). Similar changes were observed in nonculprit arteries (CFR: 2.8 ± 0.7 vs. 2.0 ± 0.7 for STEMI patients and control subjects; p < 0.001). CFR significantly correlated with infarct size as a percentage of the left ventricle in both patients (r = −0.48; p = 0.001) and swine (r = −0.61; p = 0.047). Conclusions CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction. [ABSTRACT FROM AUTHOR]

Objectives 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). Background 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. Methods 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). Results 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. Conclusions 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 FROM AUTHOR]

OBJECTIVE: Myocardial tissue perfusion is decreased in patients with cardiac syndrome X (CSX). Systemic inflammation appears to be an important contributor to the diseased microvascular network of these patients. The neutrophil-to-lymphocyte ratio (NLR) is a surrogate marker of inflammation. Accordingly, we evaluated this biomarker concerning the microvascular circulation of CSX patients. PATIENTS AND METHODS: This study included 60 consecutive patients (54.1 ± 7.8 years of age, 49 females) with CSX (typical chest pain, positive exercise stress test results, and normal coronary angiograms) and 60 consecutive ageand sex-matched control subjects. In all coronary territories, epicardial coronary flow was assessed by the Thrombolysis In Myocardial Infarction frame count (TFC) method, and myocardial tissue perfusion was assessed by the myocardial blush grade (MBG) method. Normal myocardial perfusion was accepted as an MBG score of 3 in all coronary territories. RESULTS: Patients with CSX had higher NLRs than those of control subjects (1.98 ± 0.77 vs 1.72 ± 0.55, respectively; p = 0.04). Among patients with CSX, those with impaired myocardial perfusion had higher NLRs than those with normal myocardial perfusion (2.13 ± 0.82 vs 1.71 ± 0.59, respectively; p = 0.028). There was a negative correlation between the NLR and total MBG score (p = 0.027, r = -0.29). Logistic regression analysis showed that the NLR was an independent and negative predictor of myocardial tissue perfusion (p = 0.027; Beta, -1.057; odds ratio, 2.878; 95% confidence interval, 1.129-7.335). CONCLUSIONS: Patients with CSX have high NLRs, and inflammation seems to be associated with distorted myocardial perfusion in these patients. [ABSTRACT FROM AUTHOR]

Background and purpose To analyze plasma adiponectin kinetics in patients with ST-segment elevation myocardial infarction (STEMI) treated by primary percutaneous coronary intervention (pPCI) and its association with coronary flow reserve (CFR), an index of coronary microcirculatory function. Methods A total of 96 consecutive patients with the first anterior STEMI treated by pPCI without heart failure were included. CFR was assessed on the 7th day after pPCI. Plasma adiponectin was measured on admission before pPCI, and on the 2nd and 7th day after pPCI. Results Adiponectin concentration was the highest on admission, declined to the lowest level on the 2nd day, and rose on the 7th day remaining below admission values. Impaired coronary microcirculatory function (CFR < 2) was observed in 41% of the patients. Adiponectin concentrations significantly positively correlated with CFR, and the strongest correlation was with the 2nd day adiponectin ( r = 0.489, p < 0.001). In multivariate models, adiponectin concentrations were independent predictors of impaired CFR [on admission: odds ratio (OR) 0.175, confidence interval (CI): 0.047–0.654, p = 0.010; 2nd day: OR 0.146, 95% CI: 0.044–0.485, p = 0.002; 7th day: OR 0.198, CI: 0.064–0.611, p = 0.005]. The best power to predict impaired CFR was the 2nd day adiponectin. Delta values of adiponectin (differences between adiponectin concentrations) did not correlate with CFR. Conclusions In patients with the first anterior STEMI treated by pPCI plasma adiponectin concentrations before and after pPCI are strongly associated with CFR. Our results support the hypothesis that low adiponectin, especially during the early post-pPCI period, carries the risk for impaired coronary microcirculatory function in STEMI patients. [ABSTRACT FROM AUTHOR]

Discordance between fractional flow reserve (FFR) and coronary flow velocity reserve (CFVR) may reflect important coronary pathophysiology but usually remains unnoticed in clinical practice. We evaluated the physiological basis and clinical outcome associated with FFR/CFVR discordance.We studied 157 intermediate coronary stenoses in 157 patients, evaluated by FFR and CFVR between April 1997 and September 2006 in which revascularization was deferred. Long-term follow-up was performed to document the occurrence of major adverse cardiac events: cardiac death, myocardial infarction, or target vessel revascularization. Discordance between FFR and CFVR occurred in 31% and 37% of stenoses at the 0.75, and 0.80 FFR cut-off value, respectively, and was characterized by microvascular resistances during basal and hyperemic conditions. Follow-up duration amounted to 11.7 years (Q1-Q3, 9.9-13.3 years). Compared with concordant normal results of FFR and CFVR, a normal FFR with an abnormal CFVR was associated with significantly increased major adverse cardiac events rate throughout 10 years of follow-up, regardless of the FFR cut-off applied. In contrast, an abnormal FFR with a normal CFVR was associated with equivalent clinical outcome compared with concordant normal results: 3 years when FFR <0.75 was depicted abnormal and throughout 10 years of follow-up when FFR 0.80 was depicted abnormal.Discordance of CFVR with FFR originates from the involvement of the coronary microvasculature. Importantly, the risk for major adverse cardiac events associated with FFR/CFVR discordance is mainly attributable to stenoses where CFVR is abnormal. This emphasizes the requirement of intracoronary flow assessment in addition to coronary pressure for optimal risk stratification in stable coronary artery disease. [ABSTRACT FROM AUTHOR]

Angina and myocardial ischemia without obstructive coronary artery disease are common clinical findings, often neglected for the assumption of a good prognosis. Most often, such patients are neither further investigated nor offered specific treatment beyond reassurance. However, the absence of significant coronary stenoses on angiography does not necessarily imply a “healthy” coronary tree. In such cases, myocardial ischemia may result from different types of functional disease involving the epicardial coronary arteries, the coronary microcirculation, or both; an accurate assessment of these components should be systematically performed after exclusion of organic epicardial disease because a correct diagnosis has relevant prognostic and therapeutic implications. Here we discuss the basic principles of diagnostic tests in this setting and propose a diagnostic sequence of reasonable practical implementation that may help identify patients at risk of future cardiac events. [Copyright &y& Elsevier]

Background: The whole body periodic acceleration (WBPA) system was recently developed as a passive exercise device by providing increased pulsatile shear stress for improvement of endothelial function. This study aimed to investigate the acute effects of WBPA on coronary microcirculation and glucose tolerance in patients with type 2 diabetes (T2D). Methods: The study subjects were 8 patients with T2D who underwent transthoracic Doppler echocardiography for the assessment of coronary flow reserve (CFR) before and immediately after a 45-min session of WBPA. The flow velocity in the distal portion of the left anterior descending coronary artery was measured at baseline and during adenosine infusion. The CFR represented the ratio of hyperemic to basal mean diastolic flow velocity. Results: WBPA increased CFR from 2.3 ±0.3 to 2.6±0.4 (p = 0.02). WBPA decreased serum insulin level from 26 ± 19 μg/ml to 19 ± 15 μg/ml (p = 0.01) and increased total adiponectin from 11.6 ± 7.3 μg/ml to 12.5 ± 8.0 μg/ml (p = 0.02) and high molecular weight adiponectin from 4.9 ± 3.6 μg/ml to 5.3 ±3.9 μg/ml (p = 0.03), whereas the serum glucose level was stable from 207 ± 66 mg/dl to 203 ±56 mg/dl (p = 0.8). Conclusions: This study demonstrates that a single session of WBPA treatment simultaneously improved coronary microcirculation and glucose tolerance in patients with T2D. [ABSTRACT FROM AUTHOR]

Abstract: Background and aim: Abnormal coronary microvascular circulation has been demonstrated in diabetes and is associated with increased rate of cardiovascular events. Our objective was to evaluate coronary vasoreactivity in young people with type 1 diabetes with and without microvascular complications. Methods and results: Twenty-five type 1 diabetic patients without microvascular complications (DC–), 23 with microvascular complications (DC+), and 18 control subjects (C) were studied. Coronary vasoreactivity was assessed by means of coronary flow reserve (CFR). Blood flow velocity in the left anterior descending coronary artery was measured at rest and after high-dose dipyridamole using transthoracic color-guided pulsed Doppler echocardiography. CFR was defined as the ratio of hyperaemic to resting diastolic peak flow velocities. The three groups had similar cardiac function parameters, and also systolic and diastolic blood pressure at rest, which remained unchanged during dipyridamole infusion. Resting coronary flow velocity was comparable in C, DC–, and DC+ (p =ns). Dipyridamole infusion produced a threefold increase in coronary diastolic peak velocity, which reached similar values in C (0.69±0.16m/s), DC– (0.69±0.18m/s), and DC+ (0.66±0.11m/s). Mean CFR ratio was similar in C (3.33±0.66), DC– (3.30±0.51), and DC+ (3.24±0.60). At multiple linear regression analysis, no association was found between CFR and age, sex, HbA1c, duration of diabetes, and complications. Conclusion: Coronary vasodilatory function is preserved in young D patients, even those with early microvascular complications, suggesting that coronary vasoreactivity deteriorates at more advanced stages of microvascular complications and/or in the presence of other cardiovascular risk factors. [ABSTRACT FROM AUTHOR]

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: Background and purpose: To evaluate intramyocardial coronary flow velocity pattern by transthoracic Doppler echocardiography and its clinical significance in patients with hypertrophic cardiomyopathy (HCM). Methods and results: In 48 patients with HCM who had angiographically normal coronary artery, coronary flow velocity in the left anterior descending coronary artery (LAD) and intramyocardial coronary artery (IMCA) derived from LAD were evaluated using transthoracic Doppler echocardiography. Two clearly different flow patterns in the IMCA were observed in patients with HCM. Twenty-seven HCM patients (group A) had slow deceleration slope in the IMCA flow (average diastolic deceleration time, 989±338; range, 585–1680) and the remaining 21 patients (group B) had steep deceleration slope with diastolic deceleration time <300ms, resulting in a no reflow-like pattern in the IMCA flow (average diastolic deceleration time, 166±67; range, 55–280). There were no significant differences in the clinical characteristics and LAD flow velocity profiles between the two groups. The incidence of cardiovascular symptoms (chest pain or syncope) was significantly higher in group B than in group A (67% vs. 26%, p <0.01). Additionally, exercise-induced ischemia as detected by thallium-201 scintigraphy was significantly more frequent in group B than in group A (6 of 9 (67%) vs. 0 of 9 (0%), p <0.01). Conclusions: Two different intramyocardial coronary flow velocity patterns are observed in patients with HCM using transthoracic Doppler echocardiography. No reflow-like pattern in the IMCA is strongly related to myocardial ischemia in the absence of epicardial coronary artery stenosis, suggesting that coronary microvascular dysfunction may be a causative mechanism. [Copyright &y& Elsevier]

Abstract: Background: It remains unclear whether coronary microvascular response to α-adrenergic activation alters in chronic heart failure (CHF). Methods and Results: We investigated the α-adrenergic receptor–mediated effects on coronary pressure-flow relationship (CPFR) in a tachycardia-induced canine heart failure model. The dogs studied were male (29 of 31) and the drugs were given intracoronary. The slope of CPFR during long diastole was evaluated as an index of coronary vascular resistance, during α1- or α2-adrenergic stimulation or inhibition under anesthesia in the baseline and failing state after 3 weeks of rapid ventricular pacing. Resting coronary blood flow and CPFR did not change in the failing state from the baseline state. Neither α1 nor α2 stimulation changed the slope of CPFR in the baseline state. However, in the failing state, α1 stimulation decreased the slope of CPFR by 23 ± 5% (P < .05), whereas α2 stimulation increased it by 73 ± 10% (P < .05), which was nearly abolished by pretreatment with NG-nitro-l-arginine methyl ester. Conclusion: α2-mediated vasodilatory action, presumably via endothelium-derived nitric oxide release, would be enhanced in the coronary microvascular bed, which may antagonize enhanced α1-induced vasoconstriction in CHF. [Copyright &y& Elsevier]

Copyright of Revista Española de Cardiología (18855857) is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Rationale and objectives: To develop a method to provide absolute values of regional myocardial perfusion by means of color maps, and to determine myocardial perfusion reserve using magnetic resonance imaging during the first pass of gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA).Materials and methods: The study population consisted of five patients with hypertrophic cardiomyopathy, two with dilated cardiomyopathy, four with coronary artery disease, and one with normal coronary arteries who presented with mildly abnormal electrocardiogram findings. For each heartbeat, six continuous slices were acquired during the first pass of Gd-DTPA (0.05 mmol/kg body weight) before and during adenosine triphosphate (ATP) **stress using an electrocardiogram-triggered fast low-angle shot (FLASH) sequence on a 1.5-T magnetic resonance unit. Myocardial perfusion images were created and displayed by means of a color scale. The parameters were calculated pixel by pixel, using the upslope method. Myocardial perfusion reserve was then calculated, as the quotient of myocardial perfusion during ATP stress and perfusion before ATP stress.Results: Myocardial perfusion during ATP stress in patients with normal coronary arteries (n = 1) or after successful percutaneous coronary intervention (n = 2) was increased compared with that before ATP stress. However, the patients with coronary artery disease (n = 2) failed to show increased myocardial perfusion. The patients with hypertrophic cardiomyopathy showed increased myocardial perfusion during ATP stress, although two with dilated cardiomyopathy did not.Conclusion: Our new technique can provide absolute values of regional myocardial perfusion by means of color maps, and has potential for widespread use for evaluation of ischemic and other types of heart disease. [Copyright &y& Elsevier]