Background: The aim of this study was to assess the relationship among anthropometric indexes of adiposity (body mass index BMI, waist circumference WC), endothelial progenitor cells (EPC) and ...carotid intima-media thickness (IMT) in patients with morbid obesity, and the effect of diabetes and weight loss. Methods and Results: BMI, WC, IMT and circulating EPC (defined as CD34+/KDR+/CD45- cells) were assessed in 100 patients (37 with diabetes). Fifty patients underwent bariatric surgery, and in 48 of them a complete re-assessment after an average follow-up of 252±108 days was carried out. In 29 of them subcutaneous and visceral adipose tissue samples were obtained at the time of intervention and analyzed for the presence and number of EPC. EPC were directly correlated with weight, BMI, WC and insulin level, and inversely with mean IMT. All correlations were confined to non-diabetic patients. EPC were found in both subcutaneous and visceral adipose tissue specimens. Circulating EPC significantly decreased after weight loss (P=0.002). Conclusions: EPC are positively related to markers of adiposity in severe obesity, when not complicated by diabetes. Weight loss is associated with decrease in EPC level. EPC are inversely correlated with IMT, confirming their protective role also in severe obesity. Diabetes has a negative modulating action. (Circ J 2014; 78: 977–985)
To clarify the meaning of elevated cardiac troponin in elite soccer athletes previously infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and screened for cardiovascular ...involvement in the wake of competitive sport resumption.
We designed a retrospective cohort study with the collaboration of two Italian Serie A teams. Soccer players from both rosters (58 athletes) were systematically analysed. For every SARS-CoV-2 positive athlete, the Italian Soccer Federation protocol requested full blood tests including high-sensitivity cardiac troponin I (hs-cTnI), along with a complete cardiovascular examination. We extended the analysis to SARS-CoV-2 negative athletes.
A total of 13/58 players (22.4%) suffered from SARS-CoV-2infection: all had a negative cardiovascular examination and 2/13 (15%) showed increased hs-cTnI values (120.8 pg/ml and 72,6 pg/ml, respectively; upper reference level 39.2 pg/ml), which did not track with inflammatory biomarkers. Regarding the 45/58 (77.6%) non infected athletes, a slight increase in hs-cTnI was observed in 2 (4.5%) subjects (values: 61 pg/ml and 75 pg/ml respectively). All hs-cTnI positive athletes (4/58, 7%) underwent cardiac magnetic resonance (CMR), that excluded any cardiac injury.
In our retrospective study, SARS-CoV-2 infection in elite soccer athletes was not associated to clinical or biomarkers abnormalities. Increased hs-cTnI was rare and not significantly associated with previous SARS-COV2 infection nor with pathological findings at CMR, albeit elevated hs-cTnI was numerically more prevalent in the infected group.
•The meaning of elevated hs-cTnI in elite athletes previously infected with coronavirus disease 2019 (COVID-19) is unknown.•In our cohort or previously infected professional soccer players, increased hs-cTnI was was was not associated to abnormalities at electrocardiogram and echocardiography, nor at cardiac magnetic resonance imaging.
In the expanding world of cardiovascular diseases, rapidly reaching pandemic proportions, the main focus is still on coronary atherosclerosis and its clinical consequences. However, at least in the ...Western world, middle-aged male patients with acute myocardial infarction are no more the rule. Due to a higher life expectancy and major medical advances, physicians are to treat older and frailer individuals, usually with multiple comorbidities. In this context, myocardial ischaemia and infarction frequently result from an imbalance between myocardial oxygen supply and demand—i.e., type 2 myocardial infarction (T2MI), according to the current universal definition—rather than coronary atherothrombosis. Moreover, the increasing use of high-sensitivity cardiac troponin assays has led to a heightened detection of T2MI—often causing relatively little myocardial injury—, which seems to have doubled its numbers in recent years. Nevertheless, owing to its multifaceted pathophysiology and clinical presentation, T2MI is still underdiagnosed. Perhaps more importantly, T2MI is also victim of undertreatment, as drugs that constitute the cornerstone of therapy in most cardiovascular diseases are much more unlikely to be prescribed in T2MI than in coronary atherothrombosis. In this paper, we review the recent literature on the classification, pathophysiology, epidemiology, and management of T2MI, trying to summarise the state-of-the-art knowledge about this increasingly important pathologic condition. Finally, based on the current scientific evidence, we also propose an algorithm that may be easily utilised in clinical practice, in order to improve T2MI diagnosis and risk stratification.
Thromboxane Production in Morbidly Obese Subjects Graziani, Francesca, MD; Biasucci, Luigi M., MD; Cialdella, Pio, MD ...
The American journal of cardiology,
06/2011, Letnik:
107, Številka:
11
Journal Article
Recenzirano
Postmortem studies have demonstrated that morbidly obese subjects, surprisingly, have less coronary atherosclerosis than obese subjects. However, the reasons for this apparent protection from ...atherosclerosis are not yet clear. Thromboxane A2, a marker of platelet activation, is greater in obese subjects than in lean subjects, and this might be a clue to their increased cardiovascular risk. However, data on thromboxane A2 in morbidly obese subjects are lacking; therefore, we hypothesized that lower levels of thromboxane A2 in morbidly obese subjects might play a role in their lower atherothrombotic burden. We measured the serum levels of thromboxane B2 (TxB2), a stable metabolite of thromboxane A2, high-sensitivity C-reactive protein (hs-CRP) and leptin in 17 lean subjects (body mass index BMI 22.9 ± 1.6 kg/m2 ), 25 obese subjects (BMI 32.6 ± 2.4 kg/m2 ), and 23 morbidly obese subjects (BMI 48.6 ± 7.1 kg/m2 ), without insulin resistance, diabetes, or overt cardiovascular disease. The serum TxB2 levels were lower in the lean subjects than in the obese subjects (p = 0.046) and in the morbidly obese subjects than in the lean and obese subjects (p = 0.015 and p <0.001, respectively). In contrast, the hs-CRP and leptin levels were greater in the obese than in the lean subjects (hs-CRP, p <0.001; leptin, p <0.001) and in the morbidly obese subjects than in the lean subjects (p <0.001 for both). Leptin was also higher in the morbidly obese subjects than in the obese subjects (p <0.001). TxB2 negatively correlated with leptin and BMI. hs-CRP correlated with leptin, and both also correlated with waist circumference, BMI, and homeostasis model assessment of insulin-resistance. In conclusion, insulin-sensitive morbidly obese subjects had lower levels of TxB2 than the obese subjects and lean subjects, suggesting that reduced platelet activation could play a role in the paradoxical protection of morbidly obese subjects from atherosclerosis, despite the greater levels of leptin.
Aims To investigate spontaneous polymorphonuclear neutrophils (PMNs) apoptosis in unstable angina (UA) and its association with recurrence of instability. Methods and results We compared PMNs ...apoptotic rate at 4 and 24 h in patients with UA, stable angina (SA), and controls (H) with two different protocols by flow cytometry. We measured apoptotic rate of isolated PMNs (Protocol 1) in 30 UA patients, 13 SA patients, and 34 H; and apoptosis of PMNs in whole blood culture (Protocol 2) in further 10 UA patients, 7 SA patients, and 6 H. Serum high-sensitivity C-reactive protein was also measured. Polymorphonuclear neutrophils of UA patients showed a decreased apoptotic rate compared with SA patients and H at 4 h in Protocol 1 (both P < 0.01), and at 24 h in Protocol 2 (P < 0.05 and <0.01, respectively). In overall population, a negative correlation was found between apoptotic rate at 4 h and high-sensitivity C-reactive protein levels (P < 0.01). Six among 40 patients with UA had early recurrence of symptoms and their apoptotic rate was significantly reduced compared with UA patients without recurrence of symptoms (P = 0.024). Conclusions Our study demonstrates delayed PMN apoptosis in UA. This alteration might be involved in the persistence of inflammatory activation and affects recurrence of instability.