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Abstract: Diagnostic reliability of indexations of peak exercise ST segment depression (ΔST) for heart rate reserve (HRi) or chronotropic reserve (CR) to identify significant coronary artery disease (CAD) by cycle-ergometer exercise testing has not been evaluated previously. Exercise testing by upright cycle-ergometer (25 W/3 min) were performed in consecutive patients in primary prevention with history of exercise-related chest discomfort and cardiovascular risk factors, or with overt peripheral artery disease, with or type-2 diabetes associated with two or more additional cardiovascular risk factors. Coronary angiography was performed after the test to assess significant CAD. Three different criteria for definition of inducible myocardial ischemia were tested versus significant CAD: peak ΔST≥100 μV, ST/HRi>1.69 μV/bpm or ST/CR>1.76 μV/%. Diagnostic accuracy vs. CAD of ΔST≥100 μV, of ST/HRi>1.69 μV/bpm, and of ST/CR>1.76 μV/% were 78%, 72%, and 89% respectively; sensitivity and specificity of the three criteria were 91% and 50%, 84% and 43%, 88% and 93%, respectively. Abnormal ST/CR predicted CAD independent of risk factors, pre-test probability, and more strongly than ΔST. Combination of ST/HRi and ST/CR criteria did not improve CAD prediction. In conclusions, in clinical setting in patients in primary prevention but with moderate-to-high pre-test probability of CAD, exercise testing by cycle-ergometry and use of ST/CR>1.76 μV/% showed elevated sensitivity and specificity, and the best accuracy for diagnosis of significant CAD. [Copyright &y& Elsevier]

Background: Cardiac resynchronization therapy (CRT) is a standard treatment for patients with heart failure and electrical dyssynchrony. Cardiac magnetic resonance (CMR) is the gold standard for assessing left ventricular (LV) function. However, the feasibility of using CMR with active CRT is still uncertain. Purpose: To assess the feasibility of a CRT "off‐on" protocol during CMR and measure the acute effects of CRT interruption on LV function. Methods: Patients underwent CMR before (pre‐CRT) and 6 months after (post‐CRT) an MR‐conditional CRT defibrillator implantation. The post‐CRT scan included two complete sets of cine images, one with inactive (post‐CRTOFF) and one with active CRT (post‐CRTON), maintaining a continuous connection between device and programmer. Results: Out of 29 enrolled patients, 8 (28%) had complete and analyzable post‐CRT data. Unsuccessful procedures were attributed to connection problems between the CRT device and the programmer (n = 10), poor image quality (n = 7), and lack of patient cooperation (n = 4). LV ejection fraction significantly increased between pre‐CRT scan (28.1%) and both post‐CRTOFF (37.9%; p = 0.046) and post‐CRTON CMR (35.0%; p = 0.037), with a nonstatistically significant trend toward decreased LV volumes. No adverse events or significant changes in device electrical parameters (including battery level) were detected during the post‐CMR scan period. Conclusion: A CRT "off‐on" protocol during CMR studies can be safely executed in patients with an MR‐conditional CRT defibrillator. However, technical improvements are needed to facilitate high‐quality scans during active CRT. Favorable changes in LV function induced by CRT remodeling were not acutely reversed with the interruption of electrical therapy. [ABSTRACT FROM AUTHOR]

Abstract: Background: methionine ingestion (100mg/kg) identifies subjects in whom fasting total homocysteine (tHcy) may be normal but the post-methionine load (PML) tHcy is abnormally high. Methods: In 96 subjects [54 M/42 F, 40.4±12.3yrs old; 28 with the 68bp844 ins of the Cystathionine-β-synthase gene (CBSins+); 20 homozygotes for the C677T mutation of the methylene-tetrahydrofolate reductase gene (MTHFR++); 13 with the combination of the two, and 35 without any of them], we have evaluated in vivo oxidative stress and platelet activation, as reflected by urinary excretions of 8-iso-PGF2α and of 11-dehydro-TXB2 respectively, before and after a methionine load test (PML). A history of early-onset thrombosis (18 arterial, 32 venous, 2 both) was present in 52/96 of them. Results: Baseline ; tHcy was highest in MTHFR++ carriers (p<0,05); 8-iso-PGF2α and 11-dehydro-TXB2 levels were independent of sex, MTHFR++ and/or CBSins+(p>0.05). PML ; The ~3-fold increase (p<0.01 vs baseline) in tHcy reached a plateau within 6–8hrs. Mean PML tHcy was maximal in MTHFR++ carriers (p=0.000). 8-iso-PGF2α and 11-dehydro-TXB2 increase reached a maximum within 4hrs. 11-dehydro-TXB2 increase was highest (p=0.023 vs baseline) in subjects with a history of thrombosis. Baseline 11-dehydro-TXB2 and a history of thrombosis independently predicted PML 11-dehydro-TXB2 (β=0.287, p=0.000 and β=0.308, p=0.026, respectively).The PML increase in 8-iso-PGF2α or in 11-dehydro-TXB2 were comparable in the different genotypes (p>0.05). Conclusion: regardless genotypes associated with moderate hyperhomocysteinemia, following a methionine loading test, in vivo oxidative stress and platelet activation occur, being the latter maximal in subjects with a history of early-onset thrombosis. [Copyright &y& Elsevier]

Abstract: Background: In the rat liver, growth hormone (GH) affects the synthesis of vitamin-K-dependent factors, including Protein C (prot.C) and protein S (prot.S), two natural anticoagulants that prevent hypercoagulable states. Adults with GH deficiency (GHD) are at risk of thrombotic events. High circulating levels of PAI-1 and t-PA, that reflect hypercoagulable states, may contribute to such risk. In GHD adults on replacement therapy with recombinant human GH (r-HGH), %Δ PAI-1 and %Δ t-PA are related to %Δ insulin changes. Objectives: To evaluate changes in vitamin-K-dependent factors in GHD on r-HGH replacement. Methods: In 60 GHD adults, to relate plasma levels of vitamin-K-dependent factors with those of PAI-1, t-PA and insulin before and after 6-month (6-mo) replacement therapy with r-HGH. Results: After 6-mo r-HGH replacement, %Δ insulin enhancements occurred in 36/60 subjects. PAI-1, t-PA, Prot.C, Prot.S and FVIIact did not change in them. In the 24/40 subjects that experienced %Δ insulin reductions, Prot.C (p=0.025), Prot.S (p=0.031) and FVIIact (p=0.049) decreased significantly. PAI-1 (p=0.019) and t-PA antigen (p=0.009) behaved similarly. In a multivariate analysis, %∆ PAI-1 (β=0.436, p<0.01) was the strongest predictor of %∆ prot.S, wheras %∆ t-PA (β=0.385, p<0.008) and %∆ insulin (β=0.429, p<0.004) were the strongest predictors of %∆ prot.C. In all cases, regardless of %Δ insulin changes, FII, FVII Ag and FIX levels did not change from baseline. Conclusions: In GHD adults on r-HGH replacement, changes in vitamin-K-dependent factors reflect a subtle adaptation of the natural anticoagulant system to PAI-1 and t-PA changes, via the response of insulin to r-HGH. [ABSTRACT FROM AUTHOR]

Abstract: Background: Endothelial dysfunction may be related to increased left ventricular (LV) mass due to an association between endothelial dysfunction with increased arterial load. Therefore, we evaluated whether brachial artery flow-mediated dilation (FMD) is related to global arterial load. Methods: Pulse pressure/stroke index (PP/SVi, global arterial stiffness, prognostically validated), stroke volume/PP (SV/PP, global arterial compliance), and % of the predicted SV/PP by heart rate, age and body weight (confounder-adjusted global compliance, prognostically validated) were used as LV geometry-related indices of global arterial load. Results: Compared to normotensive participants (NT, n=50), those with hypertension (HTN, n=51) had lower FMD (8.3%±5.4 vs. 12.8%±6.5), higher PP/SVi (1.24±0.34 vs. 1.04±0.28mmHg m2/ml), higher LV mass and higher relative wall thickness (all p<0.01); in contrast, SV/PP and % of predicted SV/PP did not differ between NT and HTN (all p>0.1). Impaired FMD was 3–4-fold more prevalent than LV hypertrophy or increased arterial load both in NT and in HTN. Within NT and HTN separately, PP/SVi, SV/PP and % of predicted SV/PP were comparable among tertiles of FMD. Only in NT, lower FMD was associated with higher peak exercise systolic BP (p<0.05). In multivariable regression models, FMD was not associated with indices of arterial load independently (all p>0.1). Conclusions: In young-to-middle-age subjects with cardiovascular risk factors, impaired FMD is more prevalent than traditional preclinical manifestation of cardiovascular disease, and may exist independent to increased arterial load. Thus, endothelial dysfunction assessment may refine cardiovascular risk profile and risk-reduction strategies based on detection of traditional target organ damage. [Copyright &y& Elsevier]

Background: Coronavirus disease 2019 (COVID‐19) is a recently recognized viral infective disease which can be complicated by acute respiratory stress syndrome (ARDS) and cardiovascular complications including severe arrhythmias, acute coronary syndromes, myocarditis and pulmonary embolism. The aim of the present study was to identify the clinical conditions and echocardiographic parameters associated with in‐hospital mortality in COVID‐19. Methods: This is a multicentre retrospective observational study including seven Italian centres. Patients hospitalized with COVID‐19 from 1 March to 22 April 2020 were included into study population. The association between baseline variables and risk of in‐hospital mortality was assessed through multivariable logistic regression and competing risk analyses. Results: Out of 1401 patients admitted at the participating centres with confirmed diagnosis of COVID‐19, 226 (16.1%) underwent transthoracic echocardiography (TTE) and were included in the present analysis. In‐hospital death occurred in 68 patients (30.1%). At multivariable analysis, left ventricular ejection fraction (LVEF, P <.001), tricuspid annular plane systolic excursion (TAPSE, P <.001) and ARDS (P <.001) were independently associated with in‐hospital mortality. At competing risk analysis, we found a significantly higher risk of mortality in patients with ARDS vs those without ARDS (HR: 7.66; CI: 3.95‐14.8), in patients with TAPSE ≤17 mm vs those with TAPSE >17 mm (HR: 5.08; CI: 3.15‐8.19) and in patients with LVEF ≤50% vs those with LVEF >50% (HR: 4.06; CI: 2.50‐6.59). Conclusions: TTE might be a useful tool in risk stratification of patients with COVID‐19. In particular, reduced LVEF and reduced TAPSE may help to identify patients at higher risk of death during hospitalization. [ABSTRACT FROM AUTHOR]

The incidence, characteristics, and prognosis of pulmonary embolism (PE) in Coronavirus disease 2019 (COVID-19) have been poorly investigated. We aimed to investigate the prevalence and the correlates with the occurrence of PE as well as the association between PE and the risk of mortality in COVID-19. Retrospective multicenter study on consecutive COVID-19 patients hospitalized at 7 Italian Hospitals. At admission, all patients underwent medical history, laboratory and echocardiographic evaluation. The study population consisted of 224 patients (mean age 69 ± 14, male sex 62%); PE was diagnosed in 32 cases (14%). Patients with PE were hospitalized after a longer time since symptoms onset (7 IQR 3–11 days, 3 IQR 1–6 days; p = 0.001) and showed higher D-dimers level (1819 IQR 568–5017 ng/ml vs 555 IQR 13–1530 ng/ml; p < 0.001) and higher prevalence of myocardial injury (47% vs 28%, p = 0.033). At multivariable analysis, tricuspid annular plane systolic excursion (TAPSE; HR = 0.84; 95% CI 0.66–0.98; p = 0.046) and systolic pulmonary arterial pressure (sPAP; HR = 1.12; 95% CI 1.03–1.23; p = 0.008) resulted the only parameters independently associated with PE occurrence. Mortality rates (50% vs 27%; p = 0.010) and cardiogenic shock (37% vs 14%; p = 0.001) were significantly higher in PE as compared with non-PE patients. At multivariate analysis PE was significant associated with mortality. PE is relatively common complication in COVID-19 and is associated with increased mortality risk. TAPSE and sPAP resulted the only parameters independently associated with PE occurrence in COVID-19 patients. [ABSTRACT FROM AUTHOR]

Background: Mitral valve prolapse (MVP) is characterized by an abnormal movement of the valvular apparatus which may affect the papillary muscles (PMs) function and structure. Aim of the study was to investigate abnormal PM signal in MVP by using cardiac magnetic resonance imaging (MRI). Methods and Results: We enrolled 47 consecutive patients with MVP evaluated by cardiac MRI. Additional groups included healthy volunteers, patients with moderate-to-severe mitral regurgitation (not caused by MVP) and patients with hypertrophic cardiomyopathy. Visual assessment of the PM signals was carried out and the signal intensity (SI) of both the antero-lateral and postero-medial PMs was normalized by that of the left ventricular (LV) parietal myocardium. Our results show that in the MVP group only, the PM signal intensity was significantly lower compared to the one of the LV parietal myocardium. This sign did not correlate with either LV late gadolinium enhancement or positive anamnesis for significant arrhythmias. Conclusions: In MVP patients only, PM signal is significantly reduced compared to LV parietal myocardium ("darker appearance"). The described findings are not clearly related to evidence of myocardial fibrosis, as assessed by MRI, and to previous occurrence of complex ventricular arrhythmias. [ABSTRACT FROM AUTHOR]

Calculation of left ventricular (LV) ejection fraction (EF) by Doppler stroke volume and end-diastolic volume (EDV) derived from LV diastolic diameter (LVIDD) could be reliable and feasible in clinical practice. In subjects with a wide range of LV volumes and EFs, magnetic resonance imaging (MRI) was used to evaluate the accuracy of common formulas (Teichholz and Z method) to estimate EDV from LVIDD (EDVTeich; EDVZ) versus volumetric EDV. The accuracy of simplified Doppler-EF was tested in a separate study sample versus real-time 3-dimensional (RT3D) echocardiography and versus bidimensional Simpson's method. A new equation to calculate EDV from LVIDD was derived using MRI and tested in the RT3D echo samples. Feasibility of Doppler-EF was tested in a third sample of consecutive inpatients and outpatients. In the MRI sample, EDVTeich was greater whereas EDVZ was smaller than volumetric EDV (both p <0.01); however, a quadratic equation estimated EDV from LVIDD with accuracy (R² = 0.97). In the echocardiographic sample, independent of severe segmental wall motion abnormalities, EDVTeich was greater whereas EDV using Simpson's method was smaller than RT3D EDV (all p <0.05); Doppler-EF using EDVTeich was lower compared with EF by Simpson's rule or by RT3D-EF (all p <0.01). However, RT3D-EF showed no differences compared with Doppler-EF when EDV was calculated by the novel MRI-derived equation. Feasibility was 95% for Doppler-EF and 72% using Simpson's method. In conclusion, equations estimating EDV from LVIDD affect the accuracy of simplified Doppler-EF. However, Doppler-based EF may be accurate and feasible even in the presence of LV contractile asynergy. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Left ventricular (LV) diastolic dysfunction is considered the earliest manifestation of diabetic cardiomyopathy. Whether LV abnormalities identified at rest by echocardiography predict peak exercise LV performance in uncomplicated type 1 diabetes mellitus (DM1) is largely unknown. Research design and methods: We evaluated LV size, mass, and functions and peak exercise LV performance in 25 subjects with uncomplicated DM1 (median disease duration 13.5 years, 1–30 years) and in 56 non-DM subjects (24 hypertensive (HT) and 32 normotensive (NT)). Overt coronary heart disease, significant microangiopathy and central autonomic neuropathy were minimized by exclusion criteria. Peak exercise LV stroke index (SVi), cardiac index (COi), LV ejection fraction (EF), LV end-diastolic and end-systolic volumes were assessed noninvasively. No subject was on cardiovascular medications at the time of evaluation. Results: In our study, DM1 did not show LV hypertrophy or impaired LV systolic function at rest. Prevalence of diastolic dysfunction was 8% among DM1, 18% among NT and 50% among HT. Pre-exercise heart rate, SVi, COi, and peak exercise blood pressure (BP) and heart rate were comparable among the three groups, but peak exercise LV EF, SVi and COi were lower in DM1 than in HT and NT independent to covariates (p <0.05). In separate analyses, DM1 predicted lower peak exercise SVi (B =−6.2) and COi (B =−1.6, both p <0.05) independently. Within DM1, glycated haemoglobin (HbA1c) and disease duration did not predict peak exercise LV systolic function. Conclusions: Our study suggests that uncomplicated DM1 may be associated with subnormal LV contractility reserve, which might not be predicted by LV dysfunction evaluated at rest. [Copyright &y& Elsevier]