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Background and aims: Diabetes mellitus (DM) is a risk factor for left ventricle (LV) diastolic dysfunction. Aim of this study was to investigate whether endothelial and/or autonomic dysfunction are associated with LV diastolic dysfunction in DM patients. Methods: We studied 84 non-insulin-dependent type 2 DM (T2DM) patients with no heart disease by assessing: 1) LV diastolic function by echocardiography; 2) peripheral vasodilator function, by measuring flow-mediated dilation (FMD) and nitrate-mediate dilation (NMD); 3) heart rate variability (HRV) on 24-h Holter electrocardiographic monitoring. Results: Twenty-five patients (29.8%) had normal LV diastolic function, while 47 (55.9%) and 12 (14.3%) showed a mild and moderate/severe diastolic dysfunction, respectively. FMD in these 3 groups was 5.25 ± 2.0, 4.95 ± 1.6 and 4.43 ± 1.8% (p = 0.42), whereas NMD was 10.8 ± 2.3, 8.98 ± 3.0 and 8.82 ± 3.2%, respectively (p = 0.02). HRV variables did not differ among groups. However, the triangular index tended to be lower in patients with moderate/severe diastolic dysfunction (p = 0.09) and a significant correlation was found between the E/e’ ratio and both the triangular index (r = −0.26; p = 0.022) and LF amplitude (r = −0.29; p = 0.011). Conclusions: In T2DM patients an impairment of endothelium-independent, but not endothelium-dependent, dilatation seems associated with LV diastolic dysfunction. The possible role of cardiac autonomic dysfunction in diastolic dysfunction deserves investigation in larger populations of patients.

BACKGROUND AND AIMS: Previous studies showed that troponin blood levels may increase after exercise. In this study, we assessed whether, among patients with suspected of having stable angina, the increase in troponin I (TnI) levels after exercise stress test (EST) might help identify those with obstructive coronary artery disease (CAD) and myocardial ischemia. METHODS: We performed maximal treadmill EST in 50 patients (age 64 ± 9 years; 38 men) admitted to our Cardiology Department to undergo elective coronary angiography because of a suspicion of stable angina. TnI was measured before and 12 h after EST. RESULTS: TnI increased after EST compared with baseline in the whole population (from 0.44 ± 0.76 to 0.84 ± 1.12 ng/dl, P < 0.001). No difference in TnI increase was observed between patients with obstructive CAD (n = 29; 0.61 ± 0.90-1.13 ± 1.33 ng/dl) and no obstructive CAD (NO-CAD; n = 21; 0.21 ± 0.46-0.44 ± 0.54 ng/dl; P = 0.51). There was also no significant difference in post-EST TnI increase between patients with positive EST (n = 34; 0.56 ± 0.89-1.05 ± 1.28 ng/dl) or negative EST (n = 16; 0.19 ± 0.26-0.39 ± 0.43 ng/dl; P = 0.16). Moreover, no significant difference was observed in the post-EST TnI increase among groups of patients with positive EST and obstructive CAD, positive EST and NO-CAD, negative EST and obstructive CAD and negative EST and NO-CAD (P = 0.12). No clinical or EST variable was associated with post-EST TnI increase, although there was a tendency for a greater increase in those achieving a heart rate more than 85 vs. less than 85% of maximal predicted heart rate during EST (P = 0.075). CONCLUSION: TnI increase after EST in patients with suspected stable angina is largely independent of the results of coronary angiography and EST.

OBJECTIVE: Duchenne muscular dystrophy (DMD) is an inherited X-linked recessive neuromuscular disease caused by mutations of the dystrophin gene, leading to early and progressive muscle deterioration and dilated cardiomyopathy. The aim of this investigation was to assess whether treatment with sacubitril/ valsartan (S/V) is well tolerated and may have beneficial effects in DMD patients with left ventricle (LV) dysfunction. PATIENTS AND METHODS: We administered S/V to 3 DMD patients (19-29 yeard old) with LV ejection fraction <35% at echocardiography but no symptoms of heart failure. All patients were on optimal medical therapy. S/V was initiated at a very low dose of 12/13 mg/die, after withdrawal of angiotensin-converting enzyme inhibitor therapy, and slowly titrated to the dose of 49/51 mg twice daily or the maximally tolerated dose. Clinical and echocardiographic follow-up was performed after 3, 6 and 12 months. RESULTS: At baseline, the LV ejection fraction was 32±1%. A significant improvement of LV ejection fraction was observed at 3 months (44.0±6.0%; p<0.05), which was maintained at 6 (45.7±5.0%) and 12 (43.3±3.2%) months (p<0.05 for both). No relevant side effects were reported throughout the period of the study. CONCLUSIONS: Our preliminary data suggest that, in DMD patients with reduced LV ejection fraction, S/V is safe and may improve LV function.

PURPOSE: To assess the 10-year follow-up efficacy and safety of riboflavin ultraviolet A-induced cross-linking (CXL) in a population of pediatric patients aged 18 years and younger with progressive keratoconus (KC).METHODS: The prospective longitudinal cohort study included 62 eyes of 47 keratoconic patients undergoing epithelium-off CXL who completed 10-year follow-up. The surgical procedure was performed in all patients according to the Siena (Dresden modified) protocol. Evaluation included uncorrected distance visual acuity, corrected distance visual acuity, Scheimpflug corneal tomography, and optical coherence tomography demarcation line measurement. Follow-up measurements taken up to 10 years after treatment were compared with baseline values, and statistical analysis was performed using a 2-tailed paired sample Student t test.RESULTS: Uncorrected distance visual acuity and corrected distance visual acuity improved from 0.45 to 0.23 logarithm of the minimum angle resolution (P = 0.0001) and from 0.14 to 0.1 logarithm of the minimum angle resolution (P = 0.019). KC stability was recorded after 10 years of follow-up in nearly 80% of the patients. The overall 10-year follow-up progression rate was 24% including 13 eyes of 9 patients with Kmax progression over 1 diopter and 2 eyes of 2 patients who underwent corneal grafting.CONCLUSIONS: The study demonstrates the ability of CXL to slow down KC progression in pediatric patients, improving functional performance. Long-term stability may be correlated with CXL-induced delay in corneal collagen turnover and with spontaneous age-related KC stabilization. A 24% regression rate could be contemplated in the patients who were aged 15 years and younger at the time of inclusion in the treatment protocol.

OBJECTIVE: About one-third of patients undergoing percutaneous coronary interventions (PCIs) for flow-limiting coronary stenosis continue to develop signs of myocardial ischemia (MI) during exercise stress test [EST], despite successful coronary revascularization. Coronary microvascular dysfunction is a likely major cause of the persistence of EST-induced MI in these patients.PATIENTS AND METHODS: We studied 15 patients (14 men, age 67 +/- 5 years) fulfilling the following strict inclusion criteria: (1) recent PCI (<6 months), with drug-eluting stent. of coronary artery stenoses for stable angina, with evidence of full success (no residual stenosis >20% in any vessel); (2) persistence of ST-segment depression induction during EST.After a basal investigation, patients received either ranolazine (375 mg bid) or isosorbide-5-mononitrate (ISMN, 20 mg bid) for 3 weeks in a single-blind, randomized crossover study. Clinical assessment, symptom-limited EST, echocardiographic color-Doppler. with tissue-Doppler examination, and coronary microvascular dilator response to adenosine (CFR-ADO) and cold pressor test (CFR-CPT), assessed by transthoracic echo-Doppler, were obtained at baseline and the end of the 3-week therapy with each drug.RESULTS: Compared to both baseline and ISMN, ranolazine showed a longer time to 1 mm ST-segment depression (404 +/- 116 s vs. 317 +/- 98 and 322 +/- 70 s, respectively; p<0.01). No differences were observed in coronary microvascular function and diastolic left ventricular function between the 2 drugs and compared to baseline.CONCLUSIONS: Our data show that ranolazine. but not ISMN, improved time to ischemia during EST. This effect, however, was independent of any effects on coronary microvascular and diastolic function.

Purpose: To compare visual outcomes and local tumor control between two groups of patients with amelanotic choroidal melanoma treated with brachytherapy alone, or neoadjuvant photodynamic therapy before brachytherapy. Methods: Patients diagnosed with amelanotic choroidal melanoma were recruited for the study and divided into two groups: brachytherapy alone (Group A) and photodynamic therapy preceding brachytherapy (Group B). Patients of both groups were selected to be comparable. Results: Twenty-six patients with amelanotic choroidal melanoma were enrolled in the study. Within Group B, 1 month after photodynamic therapy, ultrasonography showed reduction of tumor height in 11 patients (73.4%). The mean doses of irradiation to macula and optic nerve, at baseline were 74.37 and 52.07 Gy, whereas after photodynamic therapy there was a decrease of 17.26% (P 0.008) and 21.22% (P 0.025), respectively. In terms of visual acuity, a mean decrease of 14 ETDRS letters and 5 ETDRS letters was observed at 24 months follow-up, in Groups A and B, respectively (P 0.001). Conclusion: Photodynamic therapy as neoadjuvant therapy before brachytherapy reduces tumor thickness in 73.4% of cases. As a result, a decrease of radiation toxic effects on visual function could be obtained, without compromising disease control.

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