Determination Of Coronary Flow Reserve Research Articles

OR8-2 | Intravenous vs Intracoronary Adenosine for the Determination of Coronary Flow Reserve and Index of Microcirculatory Resistance

OR8-2 | Intravenous vs Intracoronary Adenosine for the Determination of Coronary Flow Reserve and Index of Microcirculatory Resistance

Abstract 12216: Prevalence of Coronary Microvascular Dysfunction in Patients With Angina and Known Myocardial Bridge

Introduction: Myocardial bridges are prevalent in patients with and without angina and can present a diagnostic dilemma when evaluating angina. Coronary microvascular dysfunction (CMD) is an important cause of chest pain in patients presenting with angina without obstructive CAD. The prevalence of concomitant CMD and myocardial bridge is not well described. Methods: All patients with known myocardial bridge and chest pain who underwent cardiac catheterization with bridge study at the University of Chicago Medical Center between 2020-2021 were included. All patients underwent pharmacologic testing with dobutamine with measurement of resting flow reserve (RFR). Abnormal RFR was defined as < 0.8. Some patients additionally underwent coronary physiology study with adenosine (Ado) and/or acetylcholine (Ach) with determination of coronary flow reserve (CFR), index of microvascular resistance (IMR), and spasm (for Ach). Abnormal endothelial dependent microvascular function was defined as CFR < 1.5 or IMR > 31 on Ach testing. Abnormal endothelial independent microvascular function was defined as CFR < 2.0 or IMR > 25 on Ado testing. Results: A total of 27 patients (mean age 47 + 9, 60% female) were studied. There were 18 patients with hemodynamically significant bridge of whom 13 underwent surgical unroofing and 9 patients with hemodynamically insignificant bridge of whom 3 underwent surgical unroofing. There was no significant difference in rates of endothelial dependent or independent CMD or angiographic spasm between groups. Further coronary endotype data is displayed in Table 1. Conclusion: Endothelial dependent and independent microvascular dysfunction are prevalent in patients presenting with known myocardial bridge and chest pain and rates are not affected by hemodynamic significance of the bridge. Knowledge of coronary endotype in patients with myocardial bridge may assist in tailoring therapies to improve chest pain.

Association of Isolated Coronary Microvascular Dysfunction With Mortality and Major Adverse Cardiac Events: A Systematic Review and Meta-Analysis of Aggregate Data.

BackgroundThe impact of coronary microvascular dysfunction (CMD), as diagnosed by reduced coronary flow reserve, on the outcomes of patients with symptoms of myocardial ischemia and nonobstructive coronary artery disease is poorly understood. We performed a systematic review and meta‐analysis of observational studies to determine the association of CMD with outcomes.Methods and ResultsWe searched online databases for studies where coronary flow reserve was measured invasively or noninvasively, clinical events were recorded after determination of coronary flow reserve, and the frequency of those events was reported for patients with and without CMD. The primary outcome was all‐cause mortality. The secondary outcome was major adverse cardiac events, including cardiac or cardiovascular death, nonfatal myocardial infarction, cardiac hospitalization, or coronary revascularization. Estimates of effect were calculated from crude event rates with a random‐effects model. There were 122 deaths in the 4661 patients without CMD (2.6%) and 183 deaths in the 1970 patients with CMD (9.3%). The odds ratio for mortality in patients with CMD compared with those without CMD was 3.93 (95% CI, 2.91–5.30; P<0.001). There were 167 major adverse cardiac events in the 3742 patients without CMD (4.5%) and 245 events in the 1447 patients with CMD (16.9%). The odds ratio for major adverse cardiac events in patients with CMD compared with those without CMD was 5.16 (95% CI, 2.81–9.47; P<0.001).Conclusions CMD is associated with a nearly 4‐fold increase in mortality and a 5‐fold increase in major adverse cardiac events. Future studies are needed to identify effective strategies to diagnose and treat CMD.

Chronically Increased Aldosterone In Vivo Attenuates Coronary Vasodilation to Adenosine

Adenosine‐induced coronary vasodilation is an important cardioprotective mechanism during cardiac hypoxia and ischemia and is utilized clinically for the determination of coronary flow reserve (CFR), an independent predictor of cardiac mortality. Impaired coronary vasodilation to adenosine is more common in diseases associated with inappropriate activation of the renin‐angiotensin‐aldosterone system (RAAS) and recent evidence indicates that systemic blockade of mineralocorticoid receptors (MR) improves CFR in patients with diabetes. The mechanisms underlying RAAS‐dependent attenuation of coronary adenosine‐induced vasodilation, however, remain unclear. Therefore, we hypothesized that chronic infusion of the MR agonist aldosterone would blunt coronary adenosine‐mediated vasodilation and that this would involve reduced adenosine type 2A (A2A) receptor‐dependent vasodilation. Studies were performed using 13–15 week old male C57BL/6J mice infused with either vehicle (95% EtOH in saline) or a subpressor dose of aldosterone (250 μg/kg/d) chronically for 4 weeks via osmotic minipump. After infusion, left ventricular coronary arteries were dissected and function was assessed by wire myography. Chronic infusion of aldosterone raised circulating aldosterone concentrations but did not increase heart weight. Aldosterone infusion blunted coronary vasodilation to adenosine, particularly within the range of adenosine concentrations relevant to those in vivo during cardiac hypoxia (1–10 μM), but did not reduce maximal adenosine‐induced vasodilation. Coronary vasodilation to the endothelium‐dependent vasodilator acetylcholine was also blunted by aldosterone infusion. Additional studies revealed that coronary adenosine‐induced vasodilation in the mouse is entirely dependent on activation of K+ channels and that selective activation of adenosine type 2B (A2B) receptors with BAY 60–6583 induces greater vasodilation that activation of A2A receptors with CGS‐21680. Chronic aldosterone infusion blunted coronary vasodilation in response to selective A2A, but not selective A2B, activation. RT‐PCR revealed no difference in aortic A2A and A2B gene expression. Taken together, our data demonstrate that chronic elevations of aldosterone blunt coronary vasodilation to adenosine via impaired A2A‐dependent vasodilation. This aldosterone‐dependent blunting of adenosine‐mediated vasodilation has implications for cardiac injury in response to hypoxia in states associated with inappropriate RAAS activation such as obesity and diabetes.Support or Funding InformationFunded by VHA BLR&amp;D BX002030 (SBB) and a STRIDE Undergraduate Summer Research Fellowship (MK) supported by the American Physiological Society and NIH NHLBI R25 HL115473‐01.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Mineralocorticoid receptors: an appealing target to treat coronary microvascular dysfunction in diabetes.

Cardiovascular disease (CVD), particularly coronary vascular disease, is a primary contributor to diabetes-related morbidity and mortality worldwide. Specifically, dysfunction of coronary microcirculation is common in this patient population, often occurring in the absence of or preceding epicardial coronary atherosclerosis, thereby leading to impaired coronary blood flow (CBF) regulation and increased risk of myocardial ischemia/infarct. Clinically, coronary microvascular function can be assessed by determination of coronary flow reserve (CFR) (ratio of maximal hyperemic to basal CBF), and impaired CFR is a powerful independent correlate of cardiac mortality in diabetic patients (1). Importantly, recent evidence revealed that diabetic patients with preserved CFR (above the median) have cardiac event rates similar to nondiabetic patients (1). Thus, treatment strategies designed to restore CFR (i.e., coronary microvascular function) hold promise to reduce acute and long-term cardiac mortality in patients with diabetes. Diabetes is associated with increased activation of the renin-angiotensin-aldosterone system (RAAS), and evidence suggests that the aldosterone-binding mineralocorticoid receptor (MR) contributes to obesity and diabetes-related vascular dysfunction (2,3). Even modest elevations in circulating aldosterone levels correlate with increased acute ischemic events and cardiovascular death in diabetic patients with coronary artery disease (4). Furthermore, accumulating evidence demonstrates that inhibition of angiotensin II (AngII) action, via ACE inhibition or angiotensin receptor blockade (ARB), does not appreciably lower circulating aldosterone levels, suggesting a residual role for MR activation in CVD pathogenesis (5). This is consistent with initial clinical trials demonstrating reduced mortality with MR antagonist treatment in …

Target heart rate to determine the normal value of coronary flow reserve during dobutamine stress echocardiography.

BackgroundThe determination of coronary flow reserve (CFR) is an essential concept at the moment of decision-making in ischemic heart disease. There are several direct and indirect tests to evaluate this parameter. In this sense, dobutamine stress echocardiography is one of the pharmacological method most commonly used worldwide. It has been previously demonstrated that CFR can be determined by this technique. Despite our wide experience with dobutamine stress echocardiography, we ignored the necessary heart rate to consider sufficient the test for the analysis of CFR. For this reason, our main goal was to determine the velocity of coronary flow in each stage of dobutamine stress echocardiography and the heart rate value necessary to double the baseline values of coronary flow velocity in the territory of the left anterior descending (LAD) coronary artery.MethodsA total of 33 consecutive patients were analyzed. The patients included had low risk for coronary artery disease. All the participants underwent dobutamine stress echocardiography and coronary artery flow velocity was evaluated in the distal segment of LAD coronary artery using transthoracic color-Doppler echocardiography.ResultsThe feasibility of determining CFR in the territory of the LAD during dobutamine stress echocardiography was high: 31/33 patients (94%). Mean CFR was 2.67 at de end of dobutamine test.There was an excellent concordance between delta HR (difference between baseline HR and maximum HR) and the increase in the CFR (correlation coefficient 0.84). In this sense, we found that when HR increased by 50 beats, CFR was ≥ 2 (CI 93-99.2%). In addition, 96.4% of patients reached a CFR ≥ 2 (IC 91.1 - 99%) at 75% of their predicted maximum heart rate.ConclusionsWe found that the feasibility of dobutamine stress echocardiography to determine CFR in the territory of the LAD coronary artery was high. In this study, it was necessary to achieve a difference of 50 bpm from baseline HR or at least 75% of the maximum predicted heart rate to consider sufficient the test for the analysis of CFR.

Determinants of Coronary Flow Reserve in Heart Transplantation: A Study Performed With Contrast-enhanced Echocardiography

Determination of coronary flow reserve (CFR) is increasingly being used in cardiac allograft vasculopathy (CAV). We aimed to identify determinants of CFR in heart transplantation (HT). CFR was measured by transthoracic echocardiography in 119 HT recipients (97 men, 22 women; 50 +/- 12 years of age at HT and 8 +/- 5 years post-HT). CFR was expressed as the ratio of hyperemic (adenosine infusion at a rate of 0.14 mg/kg) to basal diastolic flow velocity. Rejection scores (RS) on endomyocardial biopsy were calculated. Angiographic CAV was analyzed using a qualitative grading system. The coronary tree was divided into 17 traits and a CAV severity/diffusion index (SDI) was calculated for each patient, summing the scores assigned to all lesions. Upon multivariate analysis, CFR was related to CAV (p = 0.001), interventricular septum thickness (p = 0.01), ischemic heart disease pre-HT (p = 0.02) and SDI and SDI/segment number (p < 0.0001 and p = 0.003, respectively). In patients without CAV, CFR was related only to RS for severe grades (p = 0.01). Left ventricular hypertrophy, CAV and its severity/diffusion independently contribute to reduced CFR. In patients without angiographic CAV, CFR was only independently related to RS. Because a high rejection burden is associated with increased risk of CAV, CFR reduction may be an early marker of CAV. Microvascular dysfunction may contribute to the late morbidity and mortality seen in HT.

Comparison of myocardial contrast echocardiography derived myocardial perfusion reserve with invasive determination of coronary flow reserve

Invasive measurements of coronary flow reserve (CFR) by Doppler flow wire are an established method for determining coronary blood flow physiology. Myocardial contrast echocardiography (MCE) is a potential non-invasive method for quantifying myocardial blood flow (MBF). However, few studies have compared MCE-derived myocardial perfusion reserve (MPR) with Doppler flow wire-derived CFR, measured simultaneously in human subjects. This study aimed to correlate MCE-derived MPR with Doppler flow wire-derived CFR. Ten patients with at least two angiographically normal coronary arteries underwent simultaneous invasive Doppler flow wire measurements and MCE imaging at rest and at peak hyperaemia. Hyperaemia was induced by intravenous adenosine infusion. Doppler-derived CFR was calculated as the ratio of hyperaemic to baseline average peak red blood cell velocity. MPR was calculated as the hyperaemic to baseline ratio of the following parameters: myocardial blood volume (MBV), myocardial microbubble velocity (MMV), and MBF. MCE was performed using real-time and triggered imaging with contrast infused intravenously by bolus and continuous methods. Regardless of whether the contrast was infused by bolus or continuous methods, Doppler flow wire-derived CFR had a stronger correlation with MPR derived by MBV (r=0.8, P=0.05) than with MPR derived by microbubble velocity (r=0.3, P>0.05) or MBF (r=0.4, P>0.05). Real-time imaging with continuous infusion provided better correlation with CFR than triggered imaging methods or bolus administration. Myocardial perfusion reserve derived by real-time infusion MBV measurements correlates with Doppler flow wire-derived CFR. Therefore, MPR may be a potential surrogate for Doppler flow wire-derived CFR in patients with angiographically normal coronary arteries.

306: Coronary Flow Reserve by Contrast-Enhanced Transthoracic Echocardiography Predicts Maximal Epicardial Intimal Thickness in Heart Transplant Patients with Normal Coronary Angiogram

Cardiac allograft vasculopathy (CAV) is the main limiting factor of long-term survival after heart transplantation (HT). Several noninvasive tests have proven unsatisfactory in CAV diagnosis. We assessed the role of contrast-enhanced transthoracic echocardiography (CE-TTE) during adenosine infusion, a new noninvasive method for determination of coronary flow reserve (CFR).

Blunted coronary flow reserve in systemic sclerosis.

We investigated whether the non-invasive determination of coronary flow reserve (CFR), as evaluated by transthoracic Doppler echocardiography, might be a potential method to detect early dysfunction of cardiovascular system in patients affected by systemic sclerosis (SSc) without clinical signs or symptoms of cardiac impairment. The possible correlations between the CFR values and the duration of the disease, specific autoantibodies and cutaneous involvement subsets were investigated. Forty-four consecutive patients affected by SSc were analysed. The CFR was detected in the distal left anterior descending coronary artery by contrast-enhanced transthoracic second harmonic Doppler in all SSc patients and in 16 healthy controls. CFR was assessed at rest and during hyperaemia induced by administration of adenosine at 0.14 mg/kg/min over 5 min. The CFR was calculated as the ratio between hyperaemic (peak adenosine infusion) and resting peak diastolic velocity (PdvCFR) and resting velocity time integral (VtiCFR). Past medical history was carefully investigated. Both PdvCFR and VtiCFR were significantly reduced in SSc patients when compared with controls (P<0.0001). In particular, both PdvCFR and VtiCFR were significantly lower in patients with dSSc when compared with patients affected by lSSc (P<0.02 and P<0.04 respectively). No statistically significant correlation was found between CFR values and history of smoking, serum levels of cholesterol or triglycerides, blood pressure, age of patients, duration of SSc and serum autoantibody positivity for ANA, ACA and Scl70. CFR is often reduced in SSc patients. CFR was lower in patients with dSSc than in those affected by lSSc. A reduced CFR value should be considered an indirect sign of heart involvement in scleroderma, but its clinical and prognostic implications need to be clarified.

Echocardiographic determination of coronary flow reserve. Investigative techniques and diagnostic possibilities

Echocardiographic determination of coronary flow reserve. Investigative techniques and diagnostic possibilities

Predictors of reduced coronary flow reserve in heart transplant recipients without angiographically significant coronary artery disease.

Determination of coronary flow reserve (CFR) is increasingly used to assess the functional significance of cardiac allograft vasculopathy. Although the relation between CFR and angiographically defined vasculopathy has been studied extensively, little is known about other factors determining CFR in heart transplant recipients without significant lesions by coronary angiography. Sixty consecutive patients were studied 0.5 to 148 months after heart transplantation with intracoronary Doppler and intravascular ultrasound. An endothelium-independent CFR< or =2.5 was defined as abnormal. Stepwise logistic regression analysis was used to identify factors (demographic data of donor and recipient, lipid profile, epicardial vessel morphology by intravascular ultrasound, left ventricular hypertrophy, acute rejection episodes, and hemodynamics) potentially associated with a reduced CFR. Only the presence of left ventricular hypertrophy (48% vs. 14%, P=0.007 and P=0.023, bivariate and multivariate analysis, respectively) and higher donor ages (41+/-12 vs. 29+/-11 years, P=0.002 and P=0.013, bivariate and multivariate analysis, respectively) showed an independent association with an abnormal flow reserve. CFR in patients with left ventricular hypertrophy was reduced due to higher baseline flow velocities (27+/-11 vs. 20+/-6 cm/sec, P=0.004). Furthermore, resting flow velocity increased as a function of donor age (r=0.264, P=0.047), while hyperemic flow velocity was not different. Other patient characteristics and hemodynamics did not affect CFR. The presence of left ventricular hypertrophy and higher donor ages independently contribute to a reduced CFR in patients after heart transplantation. This reduction in CFR is due to elevated baseline flow velocities rather than to a change in hyperemic flow velocities. These findings should be taken into account for the interpretation of reduced CFR values obtained by intracoronary Doppler in heart transplant recipients without angiographically overt coronary lesions.

Noninvasive determination of coronary flow reserve with signal enhanced high resolution transthoracic Doppler color echocardiography

The feasibility of non-invasive assessment of coronary flow reserve (CFR) in the left anterior descending artery (LAD) using echo-enhanced high-resolution transthoracic color Doppler echocardiography (TTCD) was investigated. The results were compared with the degree of coronary diameter-stenosis obtained during cardiac catheterization. CFR has proven to be useful in the selection of patients undergoing invasive treatment of coronary artery disease and in estimating their prognosis. However, CFR could only be determined in everyday practice invasively during catheterization procedures. Recent development of high-resolution TTCD allows transthoracic visualization of distal LAD and supra-apical intramyocardial perforator branches, and non-invasive measurement of CFR. CFR was determined by measuring the ratio of pulsed-wave Doppler time velocity integral during adenosine-induced hyperemia (140 micrograms/kg/min i.v.) to baseline value. If Doppler signal of LAD flow was insufficiently at basal condition, an echo enhancer (Levovist) was used. 45 patients were examined by TTCD (7 MHz B-mode, 5 MHz color Doppler, 3.5 MHz PW Doppler) after coronary angiography had been performed. Group I consisted of 15 patients without heart disease, Group II of 15 patients with 40 to 70% isolated LAD diameter stenosis, and Group III of 15 patients with > 70% LAD diameter stenosis. Peripheral LAD coronary flow at baseline condition was assessed in 40 patients (88%) using TTCD. CFR could be quantified in 36/45 patients (80%), in 18 patients without echo enhancer, and in 18 patients with echo-enhancing agent. In 9/45 patients CFR could not be assessed. CFR in Group I was 3.13 +/- 0.57, in Group II 2.23 +/- 0.20 (vs Group I p < 0.01) and in Group III 1.64 +/- 0.30 (vs Group II p < 0.02). CFR of LAD can be determined in 80% of patients by the synergistic use of high-resolution TTCD combined with intravenous given ultrasound echo-enhancing agent.

Current concepts of coronary flow reserve for clinical decision making during cardiac catheterization

Measurements of coronary flow reserve, once used only for research, have gained wide acceptance as an additional diagnostic approach in the decision-making process of diagnostic cardiac catheterization and coronary interventions. Apart from the noninvasive determination of coronary flow reserve, intracoronary Doppler flow wires have facilitated decision making in the catheterization laboratory. Different techniques, unstandardized procedures, and data from uncomparable patient populations have remained a confounding factor. This review examines current concepts of coronary flow reserve as well as methodologic considerations and pitfalls. Applications of coronary flow reserve for periinterventional assessment are evaluated on the background of practical guidance. According to a detailed examination of arterial structure and function, a normal coronary flow reserve exceeds a value of 3.0. Values below 3.0 suggest involvement of microvascular disease caused by functional or structural alterations. The influences of various factors such as age, hemodynamics, hypercholesterolemia, hypertrophy, hypertension, syndrome X, and coronary artery disease are discussed in relation to the effect on coronary flow reserve. From available information, measurements of coronary flow reserve are an adjunct to current interventional technology to optimize individual patient care. Further efforts should be undertaken to incorporate these new methods into our routine clinical decision making. (Am Heart J 1998;136:136-49.)

Impaired coronary flow reserve in NIDDM: a possible role for diabetic cardiopathy in humans.

Diabetic cardiopathy represents a cardiac disorder with involvement of myocardial, interstitial, coronary, and neural structures. One of the main manifestations refers to coronary microangiopathy, which has not yet been clearly identified. Coronary hemodynamics, including the determination of coronary flow reserve, were therefore analyzed in normal subjects and in nine patients with NIDDM and clinically suspected coronary heart disease but normal coronary arteriogram. Coronary flow reserve was determined as the quotient of baseline and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.). Coronary blood flow was measured quantitatively by the argon method. Systolic left ventricular function was analyzed by ventriculography and diastolic function by M-mode and Doppler echocardiography. Twelve healthy normotensive subjects served as the control group (CON). In the diabetic patients, maximal coronary flow was significantly reduced (172 +/- 50 vs. 395 +/- 103 ml/min x 100 g; P < 0.001), and minimal coronary resistance was increased (0.60 +/- 0.19 vs. 0.24 +/- 0.06 mmHg x min x 100 g/ml; P < 0.001). Coronary reserve in the diabetic subjects was markedly reduced (1.84 +/- 0.39 vs. 4.23 +/- 0.52; P < 0.001). No difference existed with respect to myocardial oxygen consumption (12.4 +/- 2.3 vs. 11.8 +/- 2.8 ml O2/100 g x min; NS). Global systolic function was normal in all patients (ejection fraction: NIDDM 72 +/- 13 vs. CON 77 +/- 12%, NS; CI: NIDDM 3.2 +/- 0.8 vs. CON 3.3 +/- 1.2 l/min x m2, NS). Diastolic function was impaired in diabetic patients with an increase in relaxation time index (97 +/- 23 vs. 45 +/- 18 ms; P < 0.01) and an impaired diastolic inflow pattern, indicated by the ratio between early and late transmitral flow (0.75 +/- 0.14 vs. 1.66 +/- 0.13; P < 0.05). We conclude that the markedly reduced coronary flow reserve in diabetic patients may play a key role in the induction and perpetuation of coronary insufficiency in myocardial ischemia, in diastolic and systolic dysfunction, and in the initiation of diabetic cardiopathy.

Estimation of coronary flow reserve by transesophageal coronary sinus Doppler measurements in patients with syndrome X and patients with significant left coronary artery disease

This study sought to determine the feasibility of coronary sinus flow velocity analysis by transesophageal Doppler echocardiography for estimation of coronary flow reserve in patients with syndrome X and patients with coronary artery disease. Coronary flow reserve provides useful information in patients with coronary artery disease and patients with syndrome X. Current methods of measuring coronary flow reserve are invasive or require extensive laboratory equipment, or both. Transesophageal Doppler recordings of coronary sinus flow velocity before and after vasodilator application may allow noninvasive determination of coronary flow reserve. We obtained coronary sinus flow velocity recordings before and after dipyridamole administration (0.6 mg/kg body weight per 5 min) in 9 patients with syndrome X, 14 with significant left coronary artery disease and 22 age-matched control patients. We used the formula anterograde minus retrograde flow velocity time integral times heart rate as an index of coronary sinus flow. Coronary flow reserve was calculated by dividing coronary sinus flow variables after dipyridamole administration by the respective baseline values. Technically adequate recordings were obtained in 44 (98%) of 45 patients. Compared with that in the control group (2.78 +/- 0.95 [mean +/- SD]), coronary flow reserve was significantly lower in patients with syndrome X (1.21 +/- 0.23, p < or = 0.001) as well as in those with coronary artery disease (1.47 +/- 0.7, p < or = 0.001). Using a cutoff coronary flow reserve value of 1.8, sensitivity, specificity and overall predictive value of coronary flow reserve determinations were, respectively, 100%, 91% and 94% for syndrome X and 86%, 91% and 89% for coronary artery disease. Coronary flow reserve calculation by transesophageal coronary sinus flow velocity recordings is feasible in a large proportion of patients and might be useful for the noninvasive evaluation of patients with syndrome X and patients with severe left coronary artery disease.

Update in nuclear cardiology.

Imaging techniques for the noninvasive detection and evaluation of coronary artery disease continue to develop. New techniques for the quantification of myocardial blood flow by positron-emission tomography, new approaches to metabolic imaging, and new gamma camera technology have the potential to expand the scope of cardiac nuclear medicine in many facilities. Determination of the best and most cost-effective method of assessing myocardial viability in patients with advanced coronary artery disease remains of key interest with research directed at alternative 201Tl imaging protocols, fatty acid metabolism, and viability assessment with the new 99mTc-based myocardial perfusion radiopharmaceuticals. The assessment of endothelial function and determination of coronary flow reserve with 13N-ammonia positron-emission tomography may aid in the identification of preclinical atherosclerosis, and in monitoring disease progression and response to therapy. New information in radionuclide perfusion imaging in young and elderly patients and in those with interventricular conduction disturbances may allow for more accurate identification of coronary artery disease. The role of radionuclide imaging in patients with dilated cardiomyopathy continues to evolve with the development of radiolabeled chemicals of the adrenergic nervous system and their analogues, which will be helpful in the stratification of disease severity. These new imaging techniques promise to increase the accuracy of nuclear cardiology for detection of disease, assessment of function, and prognosis.

Is atrial pacing needed for determination of coronary flow reserve by parametric imaging?

Heart rate changes during determination of coronary flow by parametric imaging may influence the flow measurement. Thus, the question is whether atrial pacing is mandatory for determination of coronary flow reserve (CFR) by this technique. CFR was calculated by digital subtraction angiography (parametric imaging) in 10 patients (8 with coronary artery disease and 2 control subjects) during sinus rhythm and during atrial pacing. Flow measurements were determined in the perfusion region of the left anterior descending and circumflex coronary artery, both at rest and after maximal coronary vasodilation with 10 mg intracoronary papaverine. CFR was defined as coronary flow during hyperemia divided by coronary flow at rest. Spontaneous heart rate was 71 ± 15 min −1 at baseline, 73 ± 15 min −1 after papaverine injection and 85 ± 10 min −1 during atrial pacing. Heart rate variations during coronary arteriography were 4 ± 3 min −1 at baseline and 5 ± 4 min −1 after papaverine administration. CFR was 2.61 ± 1.01 during sinus rhythm and 2.67 ± 1.05 during atrial pacing. Mean absolute difference in CFR between sinus rhythm and atrial pacing was 0.31 ± 0.31 (12 ± 10% of CFR during pacing). Spontaneous heart rate variations during coronary arteriography are not associated with significant changes in CFR. Thus, atrial pacing is not mandatory for the determination of CFR by parametric imaging.

Coronary haemodynamics in hypertensive heart disease.

Cardiac constituents affected in arterial hypertension comprise the myocardium, interstitium and coronary circulation. With regard to coronary circulation, arterial hypertension is an important risk factor in coronary artery disease, but even in the absence of coronary artery disease, hypertensive patients frequently have angina pectoris or reveal electrocardiographic abnormalities suggestive of myocardial ischaemia due to coronary insufficiency. Under clinical conditions, determination of coronary flow reserve (dipyridamole; Argon-method) allows for the evaluation of impairment of coronary regulatory reserve. In comparison to healthy normotensives, coronary haemodynamics in hypertensive patients with microvascular angina are characterized by a severely increased minimal coronary resistance and reduced maximal coronary blood flow to dipyridamole. Accordingly, coronary reserve is markedly reduced by about 40%, and metabolic, myocardial and vascular factors may be involved in this reduction. In the compensated stage of arterial hypertension, with concentric left ventricular hypertrophy, myocardial factors, such as myocyte hypertrophy, extravascular compressing forces and functional implications of impaired relaxation, as well as metabolic factors, contribute to impairment in coronary reserve to a minor extent. The reduction in coronary flow reserve is not proportional to the elevation in left ventricular muscle mass and thus the degree of left ventricular hypertrophy does not seem to determine the reduction in vasodilator reserve directly. Thus the reduction in coronary reserve seems to be primarily the consequence of an impaired vasodilating capacity of the coronary resistance vessels, as indicated by a severely increased minimum coronary resistance to dipyridamole, i.e. a severely reduced overall coronary conductance capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Determination of coronary flow reserve by myocardial contrast echocardiography

Determination of coronary flow reserve by myocardial contrast echocardiography