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Gerald Maurer

Publications and source records attributed to Gerald Maurer.

70 records · Page 4Linked to original sources
PubMed2003

Model-based analysis of electrocardiography-gated cardiac (18)F-FDG PET images to assess left ventricular geometry and contractile function.

UNLABELLED: This study presents and evaluates a model-based image analysis method to calculate from gated cardiac (18)F-FDG PET images diastolic and systolic volumes, ejection fraction, and myocardial mass of the left ventricle. The accuracy of these estimates was delineated using measurements obtained by MRI, which was considered the reference standard because of its high spatial resolution. METHODS: Twenty patients (18 men, 2 women; mean age +/- SD, 59 +/- 12 y) underwent electrocardiography-gated cardiac PET and MRI to acquire a set of systolic and diastolic short-axis images covering the heart from apex to base. For PET images, left ventricular radius and wall thickness were estimated by model-based nonlinear regression analysis applied to the observed tracer concentration along radial rays. Endocardial and epicardial contours were derived from these estimates, and left ventricular volumes, ejection fraction, and myocardial mass were calculated. For MR images, an expert manually drew contours. RESULTS: Left ventricular volumes by PET and MRI were 101 +/- 60 mL and 112 +/- 93 mL, respectively, for end-systolic volume and 170 +/- 68 mL and 189 +/- 99 mL, respectively, for end-diastolic volume. Ejection fraction was 44% +/- 13% by PET and 46% +/- 18% by MRI. The left ventricular mass by PET and MRI was 196 +/- 44 g and 200 +/- 46 g, respectively. PET and MRI measurements were not statistically significant. A significant correlation was observed between PET and MRI for calculation of end-systolic volumes (r = 0.93, SEE = 23.4, P < 0.0001), end-diastolic volumes (r = 0.92, SEE = 26.7, P < 0.0001), ejection fraction (r = 0.85, SEE = 7.4, P < 0.0001), and left ventricular mass (r = 0.75, SEE = 29.6, P < 0.001). CONCLUSION: Model-based analysis of gated cardiac PET images permits an accurate assessment of left ventricular volumes, ejection fraction, and myocardial mass. Cardiac PET may thus offer a near-simultaneous assessment of myocardial perfusion, metabolism, and contractile function.

Adult↗
PubMed2003

Predictors of early reangiography within 30 days after coronary stenting.

BACKGROUND: A substantial number of early urgent reangiographies after coronary stenting do not reveal coronary abnormalities such as thrombosis, dissection, restenosis or side branch occlusion. The characterization of patients undergoing early reangiography may reduce the number of potentially unnecessary procedures. OBJECTIVE: To evaluate the predictors for unplanned early re- angiography on the basis of the information available at the time of stent implantation. METHODS: All 71 patients with reangiography after stent implantation between 1994 and 1998 in the Department of Cardiology at the University Hospital of Vienna, Austria, were compared with a control sample of 88 patients without early reangiography during the same period (control subjects were matched for the time point of the first intervention). The clinical and procedural variables were analyzed in this case-control study. For specification of the group with negative reangiograms, differences in clinical parameters between patients with negative versus patients with positive reangiograms were also analyzed. RESULTS: Clinical predictors for early reangiography of patients without evidence of important coronary pathology were a history of hypertension and left ventricular hypertrophy, as well as total cholesterol. The angiographic predictor was multiple vessel disease, and procedural risk factors included the left anterior descending artery as the target artery, type B and C lesions and total occlusion in the left anterior descending artery, as well as high-pressure balloon stent deployment. CONCLUSION: Clinical, angiographic and procedural variables predict the risk for unplanned early reangiography after coronary stenting. Hypertensive heart disease may mimic acute coronary events; hypertension and left ventricular hypertrophy represent independent predictors of unplanned reangiography in patients with good short-term results.

Adult↗
PubMed2002

C5a stimulates production of plasminogen activator inhibitor-1 in human mast cells and basophils.

We have recently shown that resting human mast cells (MCs) produce tissue-type plasminogen activator (t-PA) without simultaneously expressing plasminogen activator inhibitor 1 (PAI-1). In the present study we have identified the anaphylatoxin rhC5a as a potent inducer of PAI-1 expression in human MCs and basophils. In primary human skin MCs and primary blood basophils, exposure to rhC5a was followed by an increase from undetectable to significant levels of PAI-1. In addition, rhC5a induced a concentration- and time-dependent increase in PAI-1 antigen in the MC line HMC-1 and the basophil cell line KU-812 and increased the expression of PAI-1 mRNA in HMC-1. In conditioned media of HMC-1 treated with rhC5a, active PAI-1 could be detected. A simultaneous loss of t-PA activity in conditioned media from the same cells indicated that rhC5a-induced PAI-1 was capable of inhibiting the enzymatic activity of coproduced t-PA. Correspondingly, the levels of t-PA-PAI-1 complexes increased in rhC5a-treated cells. When HMC-1 cells were incubated with pertussis toxin or anti-C5a receptor antibodies, the effect of rhC5a on PAI-1 production was completely abolished. Treatment of C5a with plasmin resulted in loss of its ability to induce PAI-1 production in MCs. Considering the suggested role for MCs and components of the complement system in the development of cardiovascular diseases, we hypothesize that MCs, by producing t-PA in a resting state and by expressing PAI-1 when activated by C5a, might participate in the modulation of the balance between proteases and protease inhibitors regulating tissue injury and repair in such disease processes.

Antigens, CD↗
PubMed2002

The arylhydrocarbon receptor (AhR), but not the AhR-nuclear translocator (ARNT), is increased in hearts of patients with cardiomyopathy.

The objective of this study was to investigate the expression of the arylhydrocarbon receptor (AhR) and its partner AhR-nuclear translocator (ARNT) in left ventricle specimens from explanted hearts from patients with cardiomyopathy (CMP). Explanted hearts from 16 patients with ischemic (n=9, age 63+/-12 years) and dilative (n=7, age 54+/-12 years) CMP, undergoing heart transplantation were examined. Healthy donor hearts from five accident victims served as controls. As these donors were of younger age (32+/-11 years), additionally, donor hearts from three older accident victims (age 48+/-15 years) without clinical symptoms but with signs of ventricular hyperthrophy (n=1) or atherosclerotic lesions (n=2) were included ("pathological controls"). Expression of AhR and ARNT was analyzed using semi-quantitative immunohistochemistry, and in selected samples, Western blot- and reverse-transcription polymerase chain reaction analysis were performed to confirm AhR and ARNT expression. Immunohistological analysis revealed weak to intermediate staining of anti-AhR in control, but weak to intense staining in CMP- and "pathologic control" specimens, indicating significantly increased AhR levels in the diseased heart. Moreover, in CMP specimens, the percentage of AhR-positive cells was strongly increased. Higher anti-AhR staining was also seen in two atherosclerotic "pathologic control" specimens. In all groups, the intensity of anti-ARNT staining was more pronounced than AhR staining, but significant differences or any age-related alterations were not observed. In conclusion, the increased cellular content of AhR in left ventricular specimens from CMP patients suggests a role for AhR in heart disease.

Adult↗
PubMed2002

Intracoronary thrombectomy with the X-sizer catheter system improves epicardial flow and accelerates ST-segment resolution in patients with acute coronary syndrome: a prospective, randomized, controlled study.

BACKGROUND: In patients with acute coronary syndrome (ACS), percutaneous coronary intervention (PCI) may cause thrombus dislodgment followed by reduced flow and impaired microcirculatory function. We prospectively compared conventional PCI to a strategy of additional pretreatment using the X-sizer thrombectomy system. METHODS AND RESULTS: Sixty-six patients (51 [77%] men; 54.9+/-9.9 years) with ACS (49 with ST-elevation infarction [STEMI]) and suspected intracoronary thrombus were randomized 1:1 to pretreatment with X-sizer and conventional PCI alone. Various aspects of epicardial flow and microvascular function were studied. Baseline data were similar in both groups. Postprocedural TIMI 3 flow was obtained in 90% of X-sizer-treated patients and in 84% of controls (NS); however, corrected TIMI frame count was lower in X-sizer- treated patients (18.3+/-10.2 versus 24.7+/-14.1; P<0.05). No significant group differences were observed in final coronary flow reserve, myocardial blush grade, and myocardial dye intensity. In STEMI, the sum of ST elevation was significantly lower in X-sizer-treated patients immediately after (2.78+/-3.05 versus 6.15+/-6.32 mm; P<0.03) and 6 hours after (2.17+/-2.31 versus 4.14+/-3.7 mm; P<0.05) intervention. ST-segment resolution >50% was observed in 83% of X-sizer-treated patients and in 52% of controls (P<0.03). Multivariate analysis identified X-sizer treatment as the single independent predictor of ST-segment resolution >50% (OR 4.35; 95% CI, 1.13 to 16.9; P<0.04). Major adverse cardiac events after 30 days occurred in 2 patients in each group. CONCLUSIONS: In ACS with suspected thrombus, pretreatment with the X-sizer catheter system improves epicardial flow and accelerates ST-segment resolution compared with conventional PCI alone.

Acute Disease↗
PubMed2002

Coronary no-reflow is caused by shedding of active tissue factor from dissected atherosclerotic plaque.

Defined angiographically, no-reflow (NR) manifests as an acute reduction in coronary flow in the absence of epicardial vessel obstruction. One candidate protein to cause coronary NR is tissue factor (TF), which is abundant in atherosclerotic plaque and a cofactor for activated plasma coagulation factor VII. Scrapings from atherosclerotic carotid arteries contained TF activity (corresponding to 33.03 +/- 13.00 pg/cm(2) luminal plaque surface). Active TF was sedimented, indicating that TF was associated with membranes. Coronary blood was drawn from 6 patients undergoing coronary interventions with the distal protection device PercuSurge GuardWire (Traatek, Miami, FL). Fine particulate material that was recovered from coronary blood showed TF activity (corresponding to 91.1 +/- 62.16 pg/mL authentic TF). To examine the role of TF in acute coronary NR, blood was drawn via a catheter from coronary vessels in 13 patients during NR and after restoration of flow. Mean TF antigen levels were elevated during NR (194.3 +/- 142.8 pg/mL) as compared with levels after flow restoration (73.27 +/- 31.90 pg/mL; P =.02). To dissect the effects of particulate material and purified TF on flow, selective intracoronary injection of atherosclerotic material or purified relipidated TF was performed in a porcine model. TF induced NR in the model, thus strengthening the concept that TF is causal, not just a bystander to atherosclerotic plaque material. The data suggest that active TF is released from dissected coronary atherosclerotic plaque and is one of the factors causing the NR phenomenon. Thus, blood-borne TF in the coronary circulation is a major determinant of flow.

Angioplasty↗
PubMed2002

Long-term outcome of patients with ventricular septal defect considered not to require surgical closure during childhood.

OBJECTIVES: The purpose of the study was to assess the long-term outcome of patients with small ventricular septal defects (VSDs) considered not to require surgical closure during childhood. BACKGROUND: Although patients with small VSDs have generally been considered not to require surgery, more recent data suggest that a significant percentage of these patients develop serious problems during adult life. METHODS: A total of 229 consecutive patients (115 females) with a VSD considered too small to require surgery during childhood as defined by normal pulmonary artery pressure, less than 50% shunt, pulmonary vascular resistance < or =200 dynes x s cm(-5), no VSD-related aortic regurgitation (AR), and no symptoms and who had no additional hemodynamically relevant heart defect were followed in an adult congenital heart disease program. Physical examination, electrocardiography, and echocardiography were performed in all patients in one- to three-year intervals; exercise tests and Holter monitoring were performed in 140 and 127 patients, respectively. RESULTS: Follow-up was completed in 222 patients (97%). Mean age at last visit was 30 +/- 10 years. Spontaneous VSD closure was observed in 14 patients (6%). No patients died, four patients (1.8%) had an episode of endocarditis, of whom two required aortic valve replacement, and one additional patient (0.4%) had surgical closure for hemodynamic reasons. For 118 patients who entered the study between 1993 and 1996 and were prospectively followed for 7.4 +/- 1.2 years, event-free survival with end points defined as death, endocarditis or heart surgery was 99.1 +/- 0.8% at three years, 96.5 +/- 1.7% at six years and 95.5 +/- 1.9% at eight years. At last visit, 94.6% of all patients studied were symptom free. Left ventricular (LV) size by echocardiography was normal in 198 (89%) patients, borderline in 23 patients and definitely enlarged in only one patient. None had systolic LV dysfunction, and pulmonary artery pressure (PAP) was normal in all patients. Mean exercise capacity was 92 +/- 21% of expected, and 87% of patients had no arrhythmias on Holter monitoring, with the remainder showing benign rhythm disorders. CONCLUSIONS: Outcome in well-selected patients with a small VSD is good. Surgical closure does not appear to be required during childhood as long as left-to-right shunt is <50% and signs of LV volume overload are absent, when PAP is not elevated, and no VSD-related AR or symptoms are present.

Adolescent↗
PubMed2002

Contribution of nicotine to acute endothelial dysfunction in long-term smokers.

OBJECTIVES: The aim of this study was to determine whether nicotine, a constituent of cigarette smoke, contributes to acute endothelial dysfunction after smoking one cigarette. BACKGROUND: Animal studies suggest that nicotine might cause an impairment of endothelium-dependent vasodilation via an increase in oxidative stress. METHODS: Sixteen healthy smokers were entered into a randomized, observer-blinded crossover study comparing the effects of nicotine nasal spray (1-mg nicotine) and cigarette smoke (1-mg nicotine, 12 mg tar) on vascular reactivity in the brachial artery. Using high-resolution ultrasound, flow-mediated dilation (FMD) and endothelium-independent, nitroglycerin-induced dilation were assessed at baseline and 20 min after the administration of nicotine (spray or cigarette). RESULTS: In response to similar increases in nicotine serum levels, FMD values declined from 10.2 +/- 4.4% to 6.7 +/- 4.0% after the spray (mean difference: -3.6 +/- 2.0%, 95% confidence interval: -4.6; -2.5, p < 0.0001) and from 9.4 +/- 3.8% to 4.3 +/- 2.8% after the cigarette (-5.1 +/- 2.6%, -6.5; -3.7, p < 0.0001). Nitroglycerin-induced dilation remained similar within both periods. Performing a period effect analysis of variance, a significant influence on FMD was found for the mode of administration (p = 0.017) and the baseline value (p = 0.021). The effect on FMD was more pronounced after the cigarette than after the spray (estimated average effect difference: 1.9% FMD). Oxidation parameters did not increase significantly after nicotine spray or tobacco exposure. CONCLUSIONS: These results demonstrate that nicotine alone causes acute endothelial dysfunction, although to a lesser extent than smoking a cigarette of the same nicotine yield. However, the precise mechanisms by which nicotine leads to this altered vascular reactivity remain unclear.

Adult↗
PubMed2002

Plasminogen activator inhibitor 1 expression is regulated by the inflammatory mediators interleukin-1alpha, tumor necrosis factor-alpha, transforming growth factor-beta and oncostatin M in human cardiac myocytes.

Accumulating evidence points towards a role for proteases and protease inhibitors in tissue remodelling and repair in a variety of organs. In particular-besides the matrix metalloprotease system-the plasminogen activator (PA)/plasmin system has been implicated in these processes in the heart. Urokinase type PA (u-PA) and PA inhibitor type 1 (PAI-1) seem to modulate cardiac rupture and infarct healing. In this study we aimed to investigate whether inflammatory mediators can regulate the expression of components of the PA/plasmin system in human adult cardiac myocytes (HACM). We could demonstrate that HACM, isolated from pieces of myocardial tissue by mechanical dispersion and characterized by positive immunostaining for the cardiac markers troponin I, tropomyosin, cardiotin and myocardial muscle-actin, in vitro express PAI-1 and tissue type PA (t-PA) whereas u-PA was not detectable in these cells. PAI-1 protein production was increased up to twofold by interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha) and up to fivefold by transforming growth factor-beta (TGF-beta) and oncostatin M (OSM). Similar changes were observed in PAI-1 transcript levels after cytokine treatment. t-PA production in HACM was not affected by these agonists. No effect of these cytokines on PAI-1 production in fibroblasts isolated from human myocardial tissue was seen. In an ex vivo model we could show that incubation of pieces of human myocardial tissue with these cytokines also resulted in an increase in PAI-1 in cardiac myocytes as evidenced by immuno-histochemistry. Furthermore we found increased PAI-1 expression in myocardial tissue from a patient suffering from acute myocarditis. Thus for the first time we provide evidence that inflammatory mediators modulate PAI-1 expression in human adult cardiac myocytes in vitro and ex vivo and could demonstrate that PAI-1 expression is increased in the in vivo setting under inflammatory conditions. If the effect on PAI-1 expression brought about by IL-1alpha, TNF-alpha, TGF-beta and OSM is not only operative under in vitro and ex vivo conditions but also in the in vivo setting one could speculate that these cytokines contribute to upregulation of PAI-1 in myocardial tissue and that PAI-1, when upregulated in myocardial tissue during inflammatory processes, could serve as a defence mechanism against excessive matrix degradation by proteases. Thus we propose a role for PAI-1 produced in the heart by cardiac myocytes in cardiac remodelling and repair processes.

Cells, Cultured↗
PubMed2002

Intimal hyperplasia and coronary flow reserve after heart transplantation: association with big endothelin-1.

BACKGROUND: Endothelin, a peptide with strong vasoconstrictive and mitogenic properties, has been found to increase after cardiac transplantation. We therefore assessed the association between its precursor peptide, big endothelin-1, and intimal hyperplasia and coronary flow reserve after heart transplantation. METHODS: Thirty-five patients without hemodynamically significant coronary artery disease after heart transplantation were investigated: Average peak flow velocity in the left anterior descending artery (LAD) was assessed by intracoronary Doppler at baseline as well as after injection of adenosine; coronary flow reserve was calculated as a ratio of both and was corrected for patient age and baseline average peak flow velocity. Lumen, intima + media and total vessel area were measured by intracoronary ultrasound. The plasma concentration of big endothelin-1 in venous blood was determined by radioimmunoassay. RESULTS: Patients with elevated big endothelin-1 levels (>2 fmol/ml) tended to have a decreased corrected coronary flow reserve (2.60 +/- 0.9 vs 3.21 +/- 1.0, p = 0.078). They also had a significantly larger intima + media area (5.82 +/- 2.9 vs 2.37 +/- 2.9 mm(2), p = 0.004) and total vessel area (18.36 +/- 5.8 vs 12.81 +/- 4.8 mm(2), p = 0.012) than those with normal plasma concentrations. CONCLUSIONS: Our study suggests an association between elevated big endothelin-1 plasma levels and the development of intimal hyperplasia and reduction of coronary flow reserve after cardiac transplantation.

Adult↗
PubMed2002

HMG CoA reductase inhibitors affect the fibrinolytic system of human vascular cells in vitro: a comparative study using different statins.

1. The results of several clinical studies investigating the effect of statin therapy on the fibrinolytic system in vivo are inconclusive. We compared the effect of six different statins (atorvastatin, cerivastatin, fluvastatin, lovastatin, pravastatin, simvastatin) on components of the fibrinolytic system expressed by human vascular endothelial cells and smooth muscle cells and by the human hepatoma cell line HepG2. 2. All statins used except pravastatin significantly decreased PAI-1 production in human endothelial and smooth muscle cells. This effect was also seen in the presence of IL-1 alpha and TNF-alpha. All statins except pravastatin increased t-PA production in human smooth muscle cells. On a molar basis cerivastatin was the most effective HMG CoA reductase inhibitor used. Only simvastatin and lovastatin increased t-PA production in endothelial cells. The effects on the fibrinolytic system were reversed by mevalonate. Statins decreased mRNA levels for PAI-1 in endothelial and smooth muscle cells and increased mRNA levels for t-PA in smooth muscle cells. Statins did not affect PAI-1 expression in HepG2 cells. Cell viability was not influenced by statins in endothelial cells and HepG2 cells whereas in smooth muscle cells a cytotoxic effect was seen at high concentrations. 3. If the effects on the fibrinolytic system of vascular cells in vitro shown in this study are also operative in vivo one could speculate that by increasing t-PA and decreasing PAI-1 at sites of vascular lesions statins might reduce fibrin formation and thrombus development. Such an effect might contribute to the clinically proven benefits of statin therapy.

Cell Line↗
PubMed2002

Intraoperative transesophageal echocardiography in valve replacement surgery.

Transesophageal echocardiography (TEE) is applied widely during heart valve replacement surgery. Intraoperative TEE (IOTEE) is used to formulate the surgical plan, assess cardiac function, and evaluate surgical outcome. This review describes the methodology of IOTEE, focusing on its role in valve replacement surgery. Specific aspects, such as its role in surgical decision making, selection of the prosthetic model and size, detection and quantification of paravalvular leaks, outflow tract obstruction, and acute prosthetic valve obstruction, are discussed. Furthermore, a description of the value of IOTEE in newer procedures, such as port access surgery, is presented.

Aortic Valve↗
PubMed2002

Idiopathic eosinophilic endomyocarditis in the absence of peripheral eosinophilia.

In this case report we present two patients with unusual manifestations of eosinophilic endomyocarditis: A 69-year-old patient with a history of heart failure and ventricular fibrillation and a 16-year-old woman with ventricular fibrillation and an ECG indicating acute myocardial infarction had both normal blood eosinophil counts at the onset of symptoms. The absence of hypereosinophilia, therefore, does not exclude the presence of eosinophilic organ infiltration. Endomyocardial biopsy may be the only diagnostic procedure to identify necrotic eosinophilic endomyocarditis in patients with unexplained heart failure or ventricular fibrillation.

Adolescent↗
PubMed2002

Chlamydia pneumoniae in carotid artery atherosclerosis: a comparison of its presence in atherosclerotic plaque, healthy vessels, and circulating leukocytes from the same individuals.

BACKGROUND AND PURPOSE: There is growing clinical and experimental evidence that infections with Chlamydia pneumoniae might contribute to the development and progression of atherosclerosis. However, studies detecting the pathogen in atherosclerotic lesions examined either only atherosclerotic vessels or control vessels without atherosclerosis obtained from a different group of individuals. We analyzed atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins, and circulating leukocytes from the same individual patients for the presence of C pneumoniae. METHODS: From each of 46 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis, these samples were analyzed by nested polymerase chain reaction for C pneumoniae-specific DNA. Furthermore, we determined IgA and IgG titers specific for the pathogen and plasma levels of C-reactive protein in these patients. RESULTS: C pneumoniae DNA was detected in 86.9% of the leukocytes and in 82.6% of the atherosclerotic plaques but in only 6.5% of the saphenous veins. In 85% of patients who also had leukocytes positive for C pneumoniae, the atherosclerotic plaques were positive and the saphenous veins were negative. The presence of C pneumoniae-specific DNA in leukocytes significantly coincided with the presence of the respective DNA in the plaques of the carotid arteries (P=0.0002). No association between the presence of C pneumoniae and specific IgA or IgG levels was seen. C-reactive protein levels were significantly higher in patients with chlamydia-positive atherosclerotic plaques and with positive leukocytes than in patients with negative plaques of the carotid arteries or negative leukocytes, respectively (P<0.01, P<0.05). CONCLUSIONS: Our observation of >80% incidence of C pneumoniae in atherosclerotic plaques of the carotid artery does not prove causality between an infection with the pathogen and the development of atherosclerosis. It must be emphasized, however, that >90% of apparently healthy saphenous veins were negative for C pneumoniae. Given the structural and functional differences between veins and arteries, careful interpretation of our results regarding a possible causative role of C pneumoniae seems warranted.

Aged↗
PubMedDate not supplied

Assessment of myocardial perfusion by dynamic N-13 ammonia PET imaging: comparison of 2 tracer kinetic models.

BACKGROUND: Measurement of myocardial blood flow (MBF) by dynamic nitrogen 13 ammonia (NH(3)) positron emission tomography (PET) uses tracer kinetic modeling to analyze time-activity curves. We compared 2 commonly used models with 2 compartments (2C) and 3 compartments (3C) for quantification of MBF and coronary flow reserve (CFR). METHODS AND RESULTS: Seventy-seven patients underwent NH(3) PET at rest and during hyperemia. Time-activity curves for blood pool and myocardial segments were obtained from short-axis images of dynamic sequences. Model fitting of the 2C and 3C models was performed to estimate regional MBF. MBF values calculated by 2C and 3C models were 0.98 +/- 0.31 mL.min(-1).g(-1) and 1.11 +/- 0.37 mL.min(-1).g(-1), respectively, at rest (P < .0001) and 2.79 +/- 1.18 mL.min(-1).g(-1) and 2.46 +/- 1.02 mL.min(-1).g(-1), respectively, during hyperemia (P < .01), resulting in a CFR of 3.02 +/- 1.31 and 2.39 +/- 1.15 (P < .0001), respectively. Significant correlation was observed between the 2 models for calculation of resting MBF (r = 0.78), hyperemic MBF (r = 0.68), and CFR (r = 0.68). CONCLUSION: Measurements of MBF and CFR by 2C and 3C models are significantly related. However, quantification of MBF and CFR significantly differs between the methods. This difference needs to be considered when normal values are established or when measurements obtained with different methods need to be compared.

Adolescent↗