Peak Coronary Flow Velocity Research Articles

Aging attenuates the coronary blood flow response to cold air breathing and isometric handgrip in healthy humans

The purpose of this echocardiography study was to measure peak coronary blood flow velocity (CBV(peak)) and left ventricular function (via tissue Doppler imaging) during separate and combined bouts of cold air inhalation (-14 ± 3°C) and isometric handgrip (30% maximum voluntary contraction). Thirteen young adults and thirteen older adults volunteered to participate in this study and underwent echocardiographic examination in the left lateral position. Cold air inhalation was 5 min in duration, and isometric handgrip (grip protocol) was 2 min in duration; a combined stimulus (cold + grip protocol) and a cold pressor test (hand in 1°C water) were also performed. Heart rate, blood pressure, O(2) saturation, and inspired air temperature were monitored on a beat-by-beat basis. The rate-pressure product (RPP) was used as an index of myocardial O(2) demand, and CBV(peak) was used as an index of myocardial O(2) supply. The RPP response to the grip protocol was significantly blunted in older subjects (Δ1,964 ± 396 beats·min(-1)·mmHg) compared with young subjects (Δ3,898 ± 452 beats·min(-1)·mmHg), and the change in CBV(peak) was also blunted (Δ6.3 ± 1.2 vs. 11.2 ± 2.0 cm/s). Paired t-tests showed that older subjects had a greater change in the RPP during the cold + grip protocol [Δ2,697 ± 391 beats·min(-1)·mmHg compared with the grip protocol alone (Δ2,115 ± 375 beats·min(-1)·mmHg)]. An accentuated RPP response to the cold + grip protocol (compared with the grip protocol alone) without a concomitant increase in CBV(peak) may suggest a dissociation between the O(2) supply and demand in the coronary circulation. In conclusion, older adults have blunted coronary blood flow responses to isometric exercise.

Insulin resistance and exercise tolerance in heart failure patients: linkage to coronary flow reserve and peripheral vascular function

BackgroundInsulin resistance has been linked to exercise intolerance in heart failure patients. The aim of this study was to assess the potential role of coronary flow reserve (CFR), endothelial function and arterial stiffness in explaining this linkage.Methods39 patients with LVEF < 35% (median LV ejection fraction (LVEF) 31 (interquartile range (IQ) 26–34), 23/39 of ischemic origin) underwent echocardiography with measurement of CFR. Peak coronary flow velocity (CFV) was measured in the LAD and coronary flow reserve was calculated as the ratio between CFV at rest and during a 2 minutes adenosine infusion. All patients performed a maximal symptom limited exercise test with measurement of peak oxygen uptake (VO2peak), digital measurement of endothelial function and arterial stiffness (augmentation index), dual X-ray absorptiometry scan (DEXA) for body composition and insulin sensitivity by a 2 hr hyperinsulinemic (40 mU/min/m2) isoglycemic clamp.ResultsFat free mass adjusted insulin sensitivity was significantly correlated to VO2peak (r = 0.43, p = 0.007). Median CFR was 1.77 (IQ 1.26-2.42) and was correlated to insulin sensitivity (r 0.43, p = 0.008). CFR (r = 0.48, p = 0.002), and arterial stiffness (r = −0.35, p = 0.04) were correlated to VO2peak whereas endothelial function and LVEF were not (all p > 0.15). In multivariable linear regression adjusting for age, CFR remained independently associated with VO2peak (standardized coefficient (SC) 1.98, p = 0.05) whereas insulin sensitivity (SC 1.75, p = 0.09) and arterial stiffness (SC −1.17, p = 0.29) were no longer associated with VO2peak.ConclusionsThe study confirms that insulin resistance is associated with exercise intolerance in heart failure patients and suggests that this is partly through reduced CFR. This is the first study to our knowledge that shows an association between CFR and exercise capacity in heart failure patients and links the relationship between insulin resistance and exercise capacity to CFR.

Evaluation of coronary blood flow velocity during cardiac arrest with circulation maintained through mechanical chest compressions in a porcine model

BackgroundMechanical chest compressions (CCs) have been shown capable of maintaining circulation in humans suffering cardiac arrest for extensive periods of time. Reports have documented a visually normalized coronary blood flow during angiography in such cases (TIMI III flow), but it has never been actually measured. Only indirect measurements of the coronary circulation during cardiac arrest with on-going mechanical CCs have been performed previously through measurement of the coronary perfusion pressure (CPP). In this study our aim was to correlate average peak coronary flow velocity (APV) to CPP during mechanical CCs.MethodsIn a closed chest porcine model, cardiac arrest was established through electrically induced ventricular fibrillation (VF) in eleven pigs. After one minute, mechanical chest compressions were initiated and then maintained for 10 minutes upon which the pigs were defibrillated. Measurements of coronary blood flow in the left anterior descending artery were made at baseline and during VF with a catheter based Doppler flow fire measuring APV. Furthermore measurements of central (thoracic) venous and arterial pressures were also made in order to calculate the theoretical CPP.ResultsAverage peak coronary flow velocity was significantly higher compared to baseline during mechanical chests compressions and this was observed during the entire period of mechanical chest compressions (12 - 39% above baseline). The APV slowly declined during the 10 min period of mechanical chest compressions, but was still higher than baseline at the end of mechanical chest compressions. CPP was simultaneously maintained at > 20 mmHg during the 10 minute episode of cardiac arrest.ConclusionOur study showed good correlation between CPP and APV which was highly significant, during cardiac arrest with on-going mechanical CCs in a closed chest porcine model. In addition APV was even higher during mechanical CCs compared to baseline. Mechanical CCs can, at minimum, re-establish coronary blood flow in non-diseased coronary arteries during cardiac arrest.

Adenosine A2A receptor gene polymorphism (1976C&gt;T) affects coronary flow reserve response during vasodilator stress testing in patients with non ischemic-dilated cardiomyopathy

Patients with non ischemic-dilated cardiomyopathy (DCM) are characterized by an activation of the adenosinergic system and reduced coronary flow reserve (CFR) evaluated by transthoracic Doppler echocardiography during vasodilator adenosinergic stress (dipyridamole administration). The aim of this study was to assess whether genetic polymorphisms (263C>T and 1976C>T) of the A2(A) receptor gene affect CFR response in patients with DCM. We enrolled a group of 80 patients with DCM (55 male; age, 62±10.3 years) and 162 healthy volunteers (55 male; age, 45.1±9.5 years). Doppler-derived CFR (high-dose dipyridamole coronary diastolic peak flow velocity to resting coronary peak flow velocity ratio) of distal left anterior descending artery was determined in DCM. A2(A) receptor genotyping was determined in all patients by polymerase chain reaction-restriction fragment length polymorphism analysis. The expression of A2(A) protein and mRNA was also assessed in healthy controls. The genotype distribution of the 263C>T (P=0.5) and 1976C>T (P=0.8) polymorphisms was not significantly different between patients and controls. Patients with 1976TT genotype had significantly lower CFR value than 1976CC patients (2.3±0.7, 2.0±0.5 and 1.9±0.4, P<0.05 for CC, CT and TT genotypes, respectively). Controls who were heterozygous (P=0.02) or homozygous (P=0.001) for the T1976 allele showed a significant increase in A2(A) receptor protein. These data demonstrate that A2(A) 1976C>T polymorphism is associated with a blunted coronary vasodilatory response in patients with DCM, and support a direct consequences of this single nucleotide polymorphism for protein expression. Additional studies are needed to better define the functional role of this genetic variant as well as to clarify the potential clinical impact of genetics during pharmacological stress cardiac imaging.

45th Annual Meeting of the Association for European Paediatric Cardiology, AEPC with joint sessions with the Japanese Society of Pediatric Cardiology and Cardiac Surgery, Granada, Spain, May 18–21, 2011

Introduction: Cardiopulmonary bypass (CPB) surgery remains associated with significant cardiovascular morbidity in both pediatric and adult patients but the mechanisms are not fully clarified. Abnormalities in coronary flow and function have beensuggested to play an important role. A few prior studies suggested protective effects on coronary and myocardial function by short intravenous (i.v.) infusion of cyclosporine A prior to CPB surgery. Methods: Barrier-bred piglets (10-12 kg, n=20) were subjected to CPB with (n=10) or without (n=10) antegrade administration for 20 minutes of cardioplegic solution. Prior to surgery, half of animals from each group received 10-minute i.v. infusion of 100 mg/kg cyclosporine A. Left anterior descending coronary flow velocity responses to adenosine, serotonin, and atrial pacing, as well as left ventricular function and postsurgical vulnerability to atrial fibrillation (Afib) were assessed by intracoronary Doppler, epicardial echocardiography, and in vivo electrophysiological study, respectively. Results: Coronary peak flow velocity (cPFV) rose significantly after surgery, especially in cardioplegia group (p0.4). There was no difference in systolic myocardial function between groups at any timepoint. Conclusions: Cardioplegia during CPB surgery of piglets was associated with profound abnormalities in coronary vasomotor tone and receptor-related flow regulation, whereas arrhythmia vulnerability appeared to be comparable with that in non-cardioplegia group. In this study, intracoronary pretreatment with cyclosporine had no observable protective effect on coronary circulation or arrhythmia vulnerability after CPB surgery. (Less)

Nebivolol induces parallel improvement of left ventricular filling pressure and coronary flow reserve in uncomplicated arterial hypertension

Our aim was to analyze the effects of 3-month antihypertensive therapy by nebivolol, a beta-blocking agent with nitric oxide-mediated vasodilatory properties, on coronary flow reserve (CFR) and left ventricular filling pressure (LVFP) in uncomplicated arterial hypertension. Twenty newly diagnosed, never treated, uncomplicated hypertensive patients (14 male and six female patients, mean age = 49 years), I-II WHO grade, underwent single-blind nebivolol treatment. At baseline and at 3-month follow-up, patients underwent Doppler echocardiography including pulsed Tissue Doppler of septal mitral annulus: the ratio between transmitral E velocity and myocardial early diastolic velocity (E/Em ratio) was calculated as an index of LVFP degree. Transthoracic Doppler-derived CFR (high-dose dipyridamole coronary diastolic peak flow velocity to resting coronary peak flow velocity ratio) of distal left anterior descending artery was also determined. After 3-month nebivolol therapy, rate-pressure product decreased (P < 0.0001). No significant change of left ventricular mass index, relative wall thickness and midwall shortening was detected. Left ventricular end-diastolic diameter and stroke volume were both marginally increased. Nebivolol increased Em (P < 0.0001), reduced E/Em ratio (from 9.0 +/- 1.6 to 8.2 +/- 1.1, P < 0.0001) and enhanced CFR (from 2.07 +/- 0.2 to 2.20 +/- 0.2, P = 0.003), because of increased hyperemic coronary flow velocity (P < 0.001). CFR increase remained significant (P < 0.001) after normalizing resting and dipyridamole coronary velocities for the respective rate-pressure product. The increase of normalized CFR induced by nebivolol was related with E/Em ratio decrease (r = -0.65, P < 0.002). Nebivolol improves LVFP as well as CFR in uncomplicated hypertension. The association between changes of CFR and those of LVFP indicates a possible common denominator between improvement of coronary microvascular function and myocardial stimulation of nitric oxide release induced by the drug.

Diminished coronary flow velocity reserve and aortic distensibility in elderly patients with chest pain and negative coronary angiograms

Aging is a dominant process that alters vascular stiffness, endothelial function and coronary flow regulation. The objective of our work was to assess simultaneously the elastic properties of the descending aorta and coronary flow velocity reserve (CFR) during the same transesophageal echocardiography (TEE) in elderly patients. The following patients with normal epicardial coronary arteries were compared: 30 subjects under 55 years of age (group 1) and 17 patients over 55 years (group 2). A complete TEE examination was carried out in all patients, and the following aortic elastic properties were calculated from aortic diameter and blood pressure data: aortic elastic modulus [E(p)] and Young's circumferential static elastic modulus [E(s)]. Doppler evaluation of left anterior descending coronary flow velocity was performed in resting conditions and after administration of 0.56 mg/Kg dipyridamole over 4 min. Peak coronary flow velocities were measured at the 6th minute at maximum vasodilation. CFR was estimated as the ratio of hyperemic to basal peak diastolic coronary flow velocities. Peak hyperemic diastolic coronary flow velocities were significantly decreased (139.1+/-35.6 cm/s vs 105.7+/-39.7 cm/s, p<0.01) in patients >55 years. CFR was decreased (2.67+/-1.05 vs 2.13+/-0.56, p<0.05), whereas E(p) (in 103 mmHg, 0.59+/-0.49 vs 0.94+/-0.65, p<0.05) and E(s) (in 103 mmHg, 5.70+/-4.30 vs 8.47+/-5.14, p<0.05) were increased in patients >55 years. A correlation was found between CFR and E(p) (r=-0.20, p<0.05). CFR and aortic distensibility are altered in elderly patients. There is a relationship between these functional parameters.

Evaluation of coronary microvascular function in patients with end-stage renal disease, and renal allograft recipients

Background Approximately half of all deaths in patients with end-stage renal disease (ESRD) are due to cardiovascular diseases. Although renal transplant improves survival and quality of life in these patients, cardiovascular events significantly affect survival. We sought to evaluate coronary flow reserve (CFR), an indicator of coronary microvascular function, in patients with ESRD and in patients with a functioning kidney graft. Methods Eighty-six patients (30 with ESRD, 30 with a functioning renal allograft, and 26 controls) free of coronary artery disease or diabetes mellitus were included. Transthoracic Doppler echocardiography was used to measure coronary peak flow velocities at baseline and after dipyridamole infusion. CFR was calculated as the ratio of hyperemic to baseline diastolic peak flow velocities and was compared among the groups. Results The mean age of the study population was 36.1 ± 7.3 years. No between-group differences were found regarding age, sex, or prevalences of traditional coronary risk factors other than hypertension. Compared with the renal transplant and control groups, the ESRD group had significantly lower mean CFR values. On multivariate regression analysis, serum levels of creatinine, age, and diastolic dysfunction were independent predictors of CFR. Conclusions CFR is impaired in patients with ESRD suggesting that coronary microvascular dysfunction, an early finding of atherosclerosis, is evident in these patients. Although associated with a decreased CFR compared with controls, renal transplant on the other hand seems to have a favorable effect on coronary microvascular function.

Effects of cardiac resynchronization therapy on coronary blood flow: Evaluation by transthoracic Doppler echocardiography☆

Relatively limited and conflicting data are available on the effects of cardiac resynchronization therapy (CRT) on coronary blood flow (CBF). To investigate changes in the left anterior descending coronary artery (LAD) flow under different CRT pacing modes by means of transthoracic Doppler echocardiography (TTE). Twenty-two responders to CRT (67+/-11 years) with idiopathic dilated cardiomyopathy underwent TTE assessment of LAD flow and Tissue Velocity Imaging during 4 programming modes: intrinsic conduction (IC), right ventricular pacing (RV), simultaneous biventricular pacing (BVP), BVP with left ventricular (LV) pre-activation. Mean coronary flow velocity (CFV) was increased by simultaneous BVP (p=0.0063 vs. IC) and BVP with LV pre-activation (p<0.0001 vs. IC; p=0.027 vs. simultaneous BVP). Peak CFV and LAD flow velocity/time integral were highest during BVP with LV pre-activation. A reduction in septal-to-lateral delay and an increase in peak systolic velocity in the basal septum were observed during simultaneous BVP and BVP with LV pre-activation. In CRT responders with idiopathic dilated cardiomyopathy, an increase in LAD flow, assessed by TTE, was observed during simultaneous BVP and BVP with LV pre-activation. This was associated with an improvement in regional myocardial contraction and a decrease in intraventricular dyssynchrony.

Isolated Atrial Microvascular Dysfunction in Patients With Lone Recurrent Atrial Fibrillation

The purpose of this study was to assess atrial myocardial perfusion in patients with lone recurrent atrial fibrillation (LRAF). Although acute atrial ischemia has been implicated in the pathogenesis of atrial fibrillation, there are few data concerning human atrial myocardial perfusion and none for patients with LRAF. Sixteen patients with LRAF and 15 control subjects with suitable coronary anatomy underwent time-averaged peak coronary blood flow velocity (APV) measurements (cm/s), using a Doppler guidewire in the proximal left circumflex coronary artery (LCx) and in the left atrial circumflex branch (LACB), at baseline (b) and after adenosine administration to achieve maximal hyperemia (h). Coronary flow reserve was defined as h-APV/b-APV. Although there were no statistically significant differences in b-APV between patients with LRAF and control subjects or between the LACB and LCx, there were significant group (p = 0.002), artery (p = 0.001), and interaction (p < 0.001) effects at maximal hyperemia. In patients with LRAF, the h-APV and coronary flow reserve of the LACB (30.4 +/- 9.5 cm/s and 2.2 +/- 0.4, respectively) were significantly lower than in the LACB of the control subjects (45.8 +/- 12.8 cm/s [p < 0.001] and 2.9 +/- 0.5 [p = 0.001], respectively) or in the patients' LCx (43.0 +/- 10.9 cm/s [p = 0.001] and 3.1 +/- 0.6 [p < 0.001], respectively). This study confirms for the first time isolated atrial myocardial perfusion abnormalities in patients with LRAF and coronary flow reserve impairment, indicating that microvascular dysfunction is a pathophysiological substrate associated with this arrhythmia.

Mitral annular calcification associated with impaired coronary microvascular function

Background Mitral annular calcification (MAC) has been shown to be associated with atherosclerosis, and is a predictor of cardiovascular events. Coronary flow reserve (CFR) determined by transthoracic echocardiography has been introduced as a reliable indicator for coronary microvascular function. In this study we sought to investigate CFR in patients with and without MAC. Methods Seventy patients (mean age, 68.2 ± 6.6 years) who were free of coronary artery disease or diabetes mellitus were involved; 35 patients with MAC constituted the experimental group while 35 patients without MAC served as controls. Using transthoracic Doppler echocardiography coronary peak flow velocities were measured at baseline and after dipyridamole infusion. CFR was calculated as the ratio of hyperemic to baseline diastolic peak flow velocities. Results The clinical and demographic characteristics including age, sex, and traditional coronary risk factors did not differ between the groups ( P > .05). The mean value of CFR was significantly lower in participants with mitral annular calcification than it was in controls (2.25 ± 0.41 vs. 2.64 ± 0.57; P < .0001). Multivariable regression analysis identified MAC ( β = −0.40, P = .004), smoking ( β = −0.36, P = .007), and C-reactive protein levels ( β = −0.28, P = .04) as the independent variables significantly associated with CFR. Conclusions Our results demonstrate that CFR is impaired in patients with mitral annular calcification suggesting that coronary microvascular-endothelial dysfunction, an early finding of atherosclerosis, is present in these patients.

Acute Effect of Esmolol Intravenously on Coronary Microcirculation in Patients With Idiopathic Dilated Cardiomyopathy

Although coronary flow reserve (CFR) impairment was correlated with the prognosis of patients with idiopathic dilated cardiomyopathy (IDC) and microvascular ischemia was implicated in the progress of the disease, little is known about the effect of the established therapy with beta blockers on coronary microcirculation. The purpose of this study was to assess the effect of beta(1) blockade on coronary blood flow and CFR in patients with IDC. Fourteen patients with IDC and 10 control subjects underwent time-averaged peak coronary flow velocity (APCFV) measurements (centimeters per second) in the proximal left anterior descending coronary artery at baseline and at maximal hyperemia before and after beta(1) blockade with intravenous esmolol. CFR was defined as APCFV at maximal hyperemia/APCFV at baseline. Although there were no significant differences in APCFV at baseline between patients with IDC and controls, patients with IDC had significantly lower APCFV at maximal hyperemia than controls (54.2 +/- 12.0 vs 75.1 +/- 18.6, p <0.05) and decreased CFR (2.39 +/- 0.38 vs 3.50 +/- 0.54, respectively, p <0.05). After beta(1) blockade, a significant decrease in APCFV at baseline (19.5 +/- 3.7 vs 22.9 +/- 5.0, p <0.05) and enhancement of APCFV at maximal hyperemia (59.5 +/- 13.3 vs 54.2 +/- 12.0, p <0.05) were observed in patients with IDC, but not in control subjects, leading to significant improvement in CFR (3.06 +/- 0.40 vs 2.39 +/- 0.38, p <0.05). In conclusion, patients with IDC had alterations in coronary blood flow and decreased CFR that improved after beta(1) blockade. These alterations in microvascular function, which are partially reversed by beta blockade, may be 1 of the underlying mechanisms that contribute to the improved prognosis of patients with IDC under such therapy.

Physiologic Assessment of Coronary Artery Stenosis without Stress Tests: Noninvasive Analysis of Phasic Flow Characteristics by Transthoracic Doppler Echocardiography

We evaluated the significance of the diastolic-to-systolic blood flow velocity ratio (DSVR) determined by transthoracic Doppler echocardiography, for a physiologic assessment of the severity of coronary stenosis without stress tests, as compared with thallium 201 single photon emission computed tomography. In 95 patients undergoing thallium 201 single photon emission computed tomography for coronary artery disease, the flow velocity in the distal left anterior descending coronary artery was obtained with transthoracic Doppler echocardiography. The mean and peak DSVR values were calculated using mean and peak coronary flow velocity. DSVR was successfully measured for 82 patients (86.3%), including 33 patients with reversible perfusion defects in the left anterior descending coronary artery territories. For predicting reversible perfusion defects in thallium 201 single photon emission computed tomography, the best cut-off points were 1.5 for mean DSVR (sensitivity 81.8%, specificity 85.7%) and 1.6 for peak DSVR (sensitivity 75.7%, specificity 83.6%). Noninvasive measurement of DSVR with transthoracic Doppler echocardiography provides physiologic estimation of the left anterior descending coronary artery stenosis severity at high success rate, without stress tests.

1023-91 Relationship between β-adrenergic system polymorphisms and coronary peak flow velocity ratio in women: Analysis from the National Heart, Lung, and Blood Institute-Sponsored Women's Ischemia Syndrome Evaluation (WISE)

1023-91 Relationship between β-adrenergic system polymorphisms and coronary peak flow velocity ratio in women: Analysis from the National Heart, Lung, and Blood Institute-Sponsored Women's Ischemia Syndrome Evaluation (WISE)

Acute Chlamydia pneumoniae infection causes coronary endothelial dysfunction in pigs

Background: Coronary endothelial dysfunction contributes to the pathogenesis of acute coronary syndromes (ACSs). Acute Chlamydia pneumoniae infection has been epidemiologically associated with ACS. In this study, we investigated whether acute C. pneumoniae infection could alter the endothelial vasomotor function of porcine coronary vessels. Methods and results: Twenty pigs, 7–9 kg in weight, were inoculated intratracheally with C. pneumoniae ( n=12) or saline ( n=8), and investigated at 3 days (five infected/four non-infected) and 2 weeks (5+2 infected/four non-infected) after inoculation. The endothelium-dependent reactivity of coronary microcirculation was assessed at both time points by measuring peak coronary flow velocity (CFV) in response to bradykinin, before and after infusions with glutathione, an antioxidant, and l-arginine, a substrate for nitric oxide synthase (NOS). CFV after bradykinin was significantly decreased in infected animals at both time points. At 2 weeks, both glutathione and l-arginine significantly improved CFV after bradykinin. CFV after sodium nitroprusside (SNP) was similar in both groups. At 3 days, the relaxation responses of bradykinin-induced pre-contracted left anterior descending (LAD) coronary rings to bradykinin were significantly less in infected animals. N G-nitro- l-arginine-methyl-ester, an NOS inhibitor, had significantly greater inhibitory effect on bradykinin-induced relaxation in infected animals. Plasma nitrate–nitrite and fibrinogen, and NOS activity from LAD coronary samples were significantly increased in infected animals. Conclusion: Acute C. pneumoniae infection causes endothelial dysfunction of both resistance and epicardial coronary vessels, and favours a pro-coagulant status. These effects could in part account for the epidemiologically suggested association between acute infection and ACS.

Phasic coronary blood flow velocity pattern and flow reserve in the atrium: regulation of left atrial myocardial perfusion

ObjectivesThe purpose of this study was to assess rest and stress atrial coronary blood flow (CBF) velocity and flow reserve. BackgroundBecause of the limitations of the methods used until now for assessing myocardial perfusion (MP) in the small mass of atrial tissue, data are lacking for human atrial MP. MethodsSeventeen patients with suitable coronary anatomy underwent CBF velocity measurements with the use of a Doppler guide wire in the proximal left circumflex coronary artery (LCx) and left atrial circumflex branch (LACB), at baseline and after adenosine administration. All measurements were performed at resting heart rate and at 100 and 120 beats/min. ResultsCoronary blood flow velocity in the LACB showed a predominant systolic pattern in contrast to the diastolic pattern of the LCx. There was a disproportionate increase in baseline time-averaged peak coronary flow velocity (cm/s) between the LACB and LCx during the two levels of pacing-induced stress (16.8 ± 5.5 vs. 16.2 ± 5.1 at rest; 22.9 ± 7.9 vs. 18.4 ± 5.2 at 100 beats/min; and 27.1 ± 8.0 vs. 20.4 ± 5.1 at 120 beats/min; significant interaction, p < 0.001), but there were no significant differences in coronary flow reserve (CFR). ConclusionsCoronary blood flow in the left atrium is out of phase with that in the ventricular myocardium, showing a predominant systolic pattern. Although atrial and ventricular CFR show no significant differences at rest and with two levels of stress, the disproportionate increase in atrial blood flow velocity during stress indicates a peculiarity of atrial perfusion regulation.

Carotid intima-media thickness is correlated with impairment of coronary flow reserve in hypertensive patients without coronary artery disease.

Hypertensive individuals occasionally experience angina-like chest pain despite having angiographically normal coronary arteries, and the etiology of this phenomenon has been suggested to be associated with depressed coronary flow reserve (CFR). Carotid intima-media thickness (IMT) assessed by ultrasound is correlated with not only cerebrovascular disease but also coronary artery disease and left ventricular hypertrophy (LVH). The aim of our study was to investigate the association between CFR and carotid IMT in patients with essential hypertension. We performed transthoracic Doppler recording of diastolic coronary flow velocity in the left anterior descending coronary artery at baseline and after maximal vasodilation by adenosine triphosphate infusion in 24 normotensive subjects and 125 hypertensive patients. CFR was defined as the ratio of hyperemic to basal averaged peak coronary flow velocity. Common cardiovascular risk factors, left ventricular mass index (LVMI), relative wall thickness (RWT), and carotid IMT were evaluated. The CFR of hypertensive patients (2.55 +/- 0.52) was significantly decreased compared with that of normotensive subjects (3.15 +/- 0.45). CFR showed a significant correlation with age, systolic blood pressure, RWT, and carotid IMT. Stepwise regression analysis revealed that, among carotid IMT, LVMI and RWT, only carotid IMT was a strong and independent parameter for predicting CFR in hypertensive patients. In conclusion, B-mode ultrasound scanning of the carotid artery seemed to be of clinical value in the screening of patients with LVH and impaired microcoronary circulation. These associations may explain the links between cardiac and cerebrovascular involvements in patients with hypertension.

Coronary flow--pressure relationship distal to epicardial stenosis.

To assess the coronary flow velocity - pressure relationship distal to a stenosis, and to evaluate the influence of microvascular abnormalities on this relationship, coronary flow velocity and coronary pressure were measured simultaneously in 38 patients (42 vessels). The instantaneous peak coronary flow velocity was plotted against the simultaneous measured distal coronary pressure, and the slope of the relation in the phase of diastolic flow decrease was calculated as the flow - pressure slope index (FPSI) and the X-intercept of the slope was calculated as zero-flow pressure (Pzf). The slope of the curve increased from 2.0+/-2.6 to 4.5+/-4.1 (p<0.001) and the X-intercept decreased from 42+/-16 to 27+/-13 mmHg (p<0.001) after papaverine injection. After successful coronary intervention, Pzf increased from 23+/-10 to 35+/-11 (p<0.01) and FPSI decreased from 6.8+/-5.1 to 3.5+/-1.8 (p<0.05). Pzf was higher in patients with an old myocardial infarction. It is feasible to assess the relationship between coronary flow and pressure distal to a stenosis in the clinical setting, and the relationship may provide additional information regarding coronary microcirculation. Microvascular abnormalities may play an important role in the coronary flow - pressure relationship distal to stenosis.

Hypertension attenuates the efficacy of hypoglycemic therapy for preserving coronary flow reserve in patients with type 2 diabetes.

Impairment of coronary flow reserve (CFR) in patients with type 2 diabetes has been generally demonstrated; however, there have been few studies investigating CFR in cases of relatively well-controlled diabetes, in distinction to the influence of hypertension. The purpose of the present study was to evaluate the influence of diabetes and hypertension upon CFR in relatively well-controlled patients. This study included 12 healthy controls (C group) and 57 patients with type 2 diabetes (DM) and/or essential hypertension who were divided into three groups as follows: patients with DM (DM group; n = 24), patients with essential hypertension (HT group; n = 15), and patients with both DM and essential hypertension (DM+HT group; n = 18). We excluded patients with evidence of coronary artery disease and/or left ventricular hypertrophy. We performed transthoracic Doppler recording of diastolic coronary flow velocity (CFV) in the left anterior descending coronary artery at rest and after maximal vasodilation by adenosine infusion (140 microg/kg/min for 3 min) CFR was defined as the ratio of hyperemic to averaged basal peak CFV. The CFR (2.92 +/- 0.46) of the DM group was not decreased compared to that of the C group (2.96 +/- 0.58), although the CFR of the HT (2.33 +/- 0.25) and DM+HT (2.35 +/- 0.25) groups were significantly reduced. Left ventricular mass index, relative wall thickness, and diastolic function were worse in the HT and DM+HT groups than in the C and DM groups. Subjects with concentric left ventricular remodeling had a lower CFR than those with normal left ventricular geometry. In conclusion, adequate hyperglycemic control prevented the progression of coronary microcirculatory disturbance, but concomitant hypertension attenuated the effect.

Simple detection of severe coronary stenosis using transthoracic doppler echocardiography at rest

Coronary flow velocity can be measured by transthoracic Doppler echocardiography (TTDE). The purpose of this study was to detect severe coronary stenosis using the diastolic-to-systolic flow velocity ratio (DSVR) determined by TTDE at rest. We prospectively examined 190 consecutive patients with angina pectoris for whom coronary angiography was planned. Doppler spectral tracings of flow velocity in the distal left anterior descending artery were recorded by TTDE at rest. The mean and peak DSVR values were computed using mean and peak coronary flow velocities. DSVR measurement by TTDE at rest was performed within 24 hours before angiography, and in patients who underwent coronary intervention it was performed again within 48 hours after the intervention. The success rate for DSVR measurement by TTDE was 83.7%. There were significant differences in peak DSVR and mean DSVR between the patients with severe stenosis (percent diameter stenosis >85%) and those without severe stenosis (1.3 ± 0.4 vs 1.9 ± 0.50 and 1.2 ± 0.4 vs 1.8 ± 0.5, respectively; p <0.0001). In the 17 patients with successful intervention, DSVR was significantly increased after the procedure (mean 1.2 ± 0.1 vs 2.0 ± 0.2; peak 1.2 ± 0.2 vs 2.0 ± 0.3, respectively; p <0.0001). For percent diameter stenosis >85%, the best cut-off points were 1.6 for peak DSVR (sensitivity 79.0%, specificity 75.7%) and 1.5 for mean DSVR (sensitivity 77.0%, specificity 77.9%). Thus, DSVR measurement by TTDE is a simple, noninvasive method for detection of severe coronary stenosis at rest.