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In this association study the authors compared the insertion/deletion (I/D) angiotensin-I converting enzyme (ACE) gene polymorphism in females and males with premature myocardial infarction (MI). I/D ACE gene polymorphism was tested in 738 subjects: 302 patients with MI (151 men and 151 women) and 436 healthy subjects (207 men and 229 women). In women the ACE-DD genotype was not associated with MI (OR 1.1, 95% CI 0.6-2.1, p=0.6), whereas the ACE-DD genotype conferred a 2-fold independent risk for MI in men (95% CI=1.2-3.4; p=0.013) after adjustment for cardiovascular risk factors. The authors found evidence for the sex difference in the effect of the ACE-DD genotype on MI risk. The ACE-DD genotype conferred a 2-fold independent risk for premature MI in males. [ABSTRACT FROM AUTHOR]

Various techniques have been used in attempts to reduce interfering gastrointestinal activity in myocardial perfusion imaging (MPI); however, these approaches have yielded inconsistent results. The goal of this study was to investigate the efficacy of monitored walking, a previously unexplored technique, in reducing subdiaphragmatic activity-related artifacts during pharmacologic stress 99m Tc-tetrofosmin MPI with SPECT to improve the overall image quality. Methods: The study included patients who underwent MPI with pharmacologic stress. They were given a step counter immediately after the radiotracer injection and were randomized into a group A, with a request to walk at least 1,000 steps before imaging, and a group B, with no specific instructions about walking. The reconstructed SPECT images were assessed visually. Moderate and severe levels of subdiaphragmatic tracer activity were considered relevant for the interpretation of the scans. Additionally, myocardial and abdominal activity was semiquantitatively assessed on raw planar images, and the mean myocardium-to-abdomen count ratios were calculated. Results: We enrolled 199 patients (95 patients in group A and 104 patients in group B). Clinical characteristics did not differ significantly between the 2 groups. Patients in group A walked more steps than patients in group B ( P < 0.001), but there were no differences in the proportion of accepted scans between the 2 groups ( P = 0.41). Additionally, there were no differences in the proportion of relevant subdiaphragmatic activity between the groups ( P = 0.91). The number of steps did not impact the acceptance rate ( P = 0.29). Conclusion: A higher number of steps walked during the waiting period between pharmacologic stress and acquisition does not affect subdiaphragmatic activity-related artifacts or the proportion of accepted scans after pharmacologic stress. However, pedometer use and clear instructions motivate patients to walk while awaiting imaging. Larger studies are required to compare a higher-step-count group with a sedentary control group to assess the influence of walking on gastrointestinal artifacts in MPI., (© 2024 by the Society of Nuclear Medicine and Molecular Imaging.)

Background: The exact interaction of factors leading to myocardial dysfunction and fibrosis of the systemic right ventricle (SRV) is not completely understood. Myocardial ischemia and injury associated with a supply-demand mismatch of the pressure overloaded SRV are thought to play an important role, however studies confirming this are lacking., Methods: Adult SRV patients were included in this single centre cohort study. All patients underwent a comprehensive diagnostic and imaging workup. A two-day stress-rest SPECT was performed to assess myocardial perfusion. SRV ischemia was defined as decreased segmental tracer uptake during exercise with significant improvement at rest. Contrast enhanced cardiac magnetic resonance imaging (CMR) was also performed in a subgroup of patients without contraindication, to assess focal myocardial fibrosis. Differences between patients with and without SRV ischemia were assessed., Results: Twenty-three SRV patients (15 with transposition of the great arteries after atrial switch procedure and 8 with congenitally corrected transposition of the great arteries; 5 (22%) females; mean age 38 ± 11 years) were included. Seven (30%) patients had SRV ischemia on SPECT. Late gadolinium enhancement on CMR was more common in patients with SRV ischemia (p = 0.002). However, there was no association between SRV ischemia and different echocardiographic or CMR parameters of SRV systolic function, laboratory markers (high-sensitivity troponin I and NT-proBNP) and exercise capacity., Conclusions: Our multimodality study showed that SRV ischemia in adult SRV patients was associated with more focal myocardial fibrosis, but not with functional or imaging markers of SRV function., Competing Interests: Declaration of Competing Interest The authors report no relationships that could be construed as a conflict of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Aims: Non-compaction cardiomyopathy (NCM) is a congenital heart disease characterized by an arrest of the myocardial compaction process. Although NCM patients have impaired formation of microvasculature, the functional impact of these changes remains undefined. We sought to analyse a potential correlation between myocardial ischemia and heart failure severity in NCM patients., Methods and Results: We enrolled 41 NCM patients (28 male and 13 female), aged 21-70 years. In all patients, we have determined left ventricular end-diastolic volume (LVEDV), left ventricular ejection fraction (LVEF), and global longitudinal strain (GLS) by echocardiography. At the same time, serum levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) have been measured, and myocardial single-photon emission computed tomography at rest and on stress was used to define significant myocardial ischemia defined as summed difference score ≥ 2. Myocardial ischemia has been demonstrated in 11 patients (27%, Group A), and 30 patients showed no significant ischemic changes (73%, Group B). The groups did not differ in sex, age, kidney, or liver function. When compared with Group B, Group A had significantly lower LVEF (35 ± 15% in Group A vs. 53 ± 11% in Group B, P < 0.001), higher LVEDV (188 ± 52 mL vs. 136 ± 52 mL, P = 0.007), lower GLS (-9.9 ± 5.2% vs. -14.5 ± 4.1%, P = 0.001), and higher NT-proBNP levels (1691 ± 1883 pg/mL vs. 422 ± 877 pg/mL, P = 0.006). Overall, higher summed difference score was associated with lower LVEF (r = -0.48, P = 0.001), higher LVEDV (r = 0.39, P = 0.012), lower GLS (r = 0.352, P = 0.024), and higher levels of NT-proBNP (r = 0.66, P < 0.001)., Conclusions: The presence of myocardial ischemia in patients with NCM is associated with worse left ventricular function, dilation of the left ventricle, and more pronounced neurohumoral activation., (© 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Objective: To test the hypothesis that, in the initial evaluation of patients with suspected coronary artery disease (CAD), stress myocardial perfusion imaging (MPI) would result in less downstream testing than coronary computed tomographic angiography (CCTA)., Methods: In this international, randomized trial, mildly symptomatic patients with an intermediate likelihood of having CAD, and asymptomatic patients at intermediate risk of cardiac events, underwent either initial stress-rest MPI or CCTA. The primary outcome was downstream noninvasive or invasive testing at 6 months. Secondary outcomes included cumulative effective radiation dose (ERD) and costs at 12 months., Results: We recruited 303 patients (151 MPI and 152 CTA) from 6 centers in 6 countries. The initial MPI was abnormal in 29% (41/143) and CCTA in 56% (79/141) of patients. Fewer patients undergoing initial stress-rest MPI had further downstream testing at 6 months (adjusted OR 0.51, 95% CI 0.28-0.91, P = 0.023). There was a small increase in the median cumulative ERD with MPI (9.6 vs. 8.8 mSv, P = 0.04), but no difference in costs between the two strategies at 12 months., Conclusion: In the management of patients with suspected CAD, a strategy of initial stress MPI is substantially less likely to require further downstream testing than initial testing with CCTA., Trial Registration: clinicaltrials.gov identification number NCT01368770.

Background: Determination of the optimal amputation level is essential for patients, morbidity and rehabilitation. Various non-invasive procedures have been proposed to determine the optimal level of amputation. There is no consensus on the minimal tcPO2 level that is required to predict the healing of the stump. Therefore we aimed to rank the probability of primary wound healing at the most distal level and to answer the question if there is a lower limit of tcPO2 below which healing cannot occur., Patients and Methods: 56 consecutive patients undergoing amputation below the knee for ischaemic gangrene of limbs were prospectively enrolled in the study. 39 were men (18 of whom were diabetics) and 17 women (8 diabetics) whose ages ranged from 45 to 87 years (mean 73 years). The total of 71 amputations was performed on the 56 patients: 39 below-knee with primary healing and, in 16 patients the above-knee reamputation was performed, due to the non-healing wound on the below-knee stump. The level of the amputation (below or above the knee) was in all cases decided solely on clinical grounds. TcPO2 was measured on each patient prior to amputation, on the dorsum of the foot and 10 cm below the knee., Results: The median tcPO2 value on the dorsum of the foot of diseased legs before amputation was 12 mm Hg (range from 0 to 22 mm Hg). At the anticipated level of the amputation of the shank, the median value of tcPO2 was 28 mm Hg (8-56 mm Hg). Patients with primary healing of postoperative wounds had significantly higher values of tcPO2 than patients with fialure to heal (37 mm Hg; range 15-56 mm Hg vs. 18 mm Hg; range 8-36 mm Hg, p < 0.01). The success rate increased with higher tcPO2 values at the level of amputation. The 15% prevalence of reamputations was obtained for tcPO2 values between 25 and 36 mm Hg (median value 33 mm Hg) and the threshold value of tcPO2 below which the stump failed to heal was 15 mm Hg., Conclusions: Our study showed that tcPO2 is a reliable indicator of local ischemia. The integration of this parameter with other personal clinical criteria may be a valuable help to the surgeon in decision making.

The pathogenesis of CAD is similar in man and woman, yet some risk factors have a greater impact on the CAD risk in woman than in man. In this study we assessed the effect of the apoE gene polymorphism on lipid metabolism and risk for CAD in women younger than 65 years (premature CAD). In a cross-sectional case-control study, 147 female Caucasian patients with premature CAD (confirmed by coronarography) were compared with a control group of 114 healthy Caucasian women. The apoE allele frequencies of patients vs. controls were 5.1% vs. 5.7% for 2, 85.4% vs. 83.3% for 3, and 9.5% vs. 11% for epsilon4. The subjects with epsilon2/3 genotype had statistically significantly higher triglycerides levels than the subjects with epsilon3/3 genotype (2.23 +/- 2.13 mmol.L(-1) vs. 1.73 +/- 0.84 mmol.L(-1); p<0.05). Logistic regression analysis revealed no association between risk genotypes (3/4 and 4/4) of the apoE gene polymorphism and CAD risk (OR 0.9; 95% CI 0. 5-1.7, P=0.7). We observed metabolic clustering of diabetes mellitus, arterial hypertension, higher BMI and triglycerides, and lower HDL cholesterol in the CAD group compared to the control group. Arterial hypertension, diabetes, HDL cholesterol level, and BMI were independent risk factors for premature CAD in female population, whereas, the risk genotype of the apoE gene polymorphism was not. In conclusion, in Slovene women risk genotypes of the apoE gene polymorphism are not associated with premature CAD; a metabolic clustering of diabetes, HDL, triglycerides and arterial hypertension is frequently present in Caucasian women with premature CAD.

Acute myocardial infarction (AMI) is more frequent in winter months than in summer months. The aetiologic mechanisms underlying this seasonal pattern are poorly understood. We investigate whether seasonal variation of metabolic and haemostatic coronary risk factors exists, and whether this variation is more pronounced in subjects with coronary artery disease (CAD). In 82 subjects (47 free of clinical signs of CAD and in 35 survivors of AMI), measurements of body mass index (BMI), lipoproteins, glucose, insulin, plasminogen activator inhibitor-1, tissue-type plasminogen activator (t-PA), euglobulin clot lysis time, fibrinogen, and platelet count were performed twice in the cold months (December and March) and twice in the warm months (June and September). Significantly higher BMI (26.8 versus 26.2 kg/m2, P < 0.01), glucose (5.5 versus 5.1 mmol/l, P < 0.01), total cholesterol (5.61 versus 5.32 mmol/l, P < 0.05), low-density lipoprotein cholesterol (3.63 versus 3.34 mmol/l, P < 0.05), triglycerides (1.79 versus 1.61 mmol/l, P < 0.01), Lp(a) (270.7 versus 237.5 mg/l, P < 0.01), fibrinogen level (3.50 versus 2.95 g/l, P < 0.00001), platelet count (212 x 10(9) versus 173 x 10(9)/l, P < 0.01) and significantly lower high-density lipoprotein cholesterol level (1.22 versus 1.28 mmol/l, P < 0.05) were observed in the cold months compared with the warm months. Significant seasonal variation of t-PA activity (1.19 versus 0.87 IU/ml, P = 0.015) and t-PA antigen (8.5 versus 7.3 ng/ml, P = 0.05) was demonstrated only in subjects with CAD. Clustering of peak values of several metabolic and haemostatic coronary risk factors was observed in winter months. This variation might be of aetiopathogenetic importance for the seasonal pattern of acute myocardial infarction.

A characteristic feature of patients with heterozygous familial hypercholesterolemia (FH) is the premature occurrence of coronary artery disease because of elevated LDL cholesterol levels. Hyperinsulinemia and insulin resistance, important characteristics of the cardiovascular dysmetabolic syndrome (CDS), were found to be associated with coronary artery disease in FH subjects, as in the general population. We investigated whether hypofibrinolysis, as part of CDS, is independently associated with symptomatic coronary artery disease in these high-risk patients. Clinical examination (body mass index, waist circumference, blood pressure) and blood analysis (plasma tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI-1) antigen and activity, fibrinogen, serum lipids and lipoproteins, fasting glucose and insulin) were carried out in 39 male patients with heterozygous FH (aged 46.6 +/- 8.8 years). Insulin resistance was calculated using the homeostasis model assessment (HOMA) mathematical model. Thirteen of the patients had suffered a myocardial infarction (MI) 5 to 8 years ago (aged 47.8 +/- 6.1 years) and 26 were free of coronary artery disease (aged 45.9 +/- 9.9 years). There was no difference in total and LDL cholesterol between the two groups. Patients with previous myocardial infarction had significantly higher levels of insulin, insulin resistance, triglycerides, t-PA antigen, PAI-1 antigen and activity, and significantly lower values of HDL cholesterol. Other widely recognised risk factors for coronary artery disease, such as smoking, systolic and diastolic blood pressure, obesity and age, did not differ significantly between the groups. In the logistic regression model, PAI-1 antigen, as a marker of hypofibrinolysis, emerged as an independent risk factor for the occurrence of myocardial infarction (odds ratio 1.55; p = 0.02). In summary our results suggest that the impairment of fibrinolytic activity resulting from elevated levels of PAI-1 antigen and activity and t-PA antigen is an independent variable in CDS associated with the premature occurrence of myocardial infarction in male patients with FH.