Aims To evaluate the impact of the COVID-19 pandemic on patient admissions to Italian cardiac care units (CCUs). Methods and Results We conducted a multicentre, observational, nationwide survey to collect data on admissions for acute myocardial infarction (AMI) at Italian CCUs throughout a 1 week period during the COVID-19 outbreak, compared with the equivalent week in 2019. We observed a 48.4% reduction in admissions for AMI compared with the equivalent week in 2019 (P < 0.001). The reduction was significant for both ST-segment elevation myocardial infarction [STEMI; 26.5%, 95% confidence interval (CI) 21.7–32.3; P = 0.009] and non-STEMI (NSTEMI; 65.1%, 95% CI 60.3–70.3; P < 0.001). Among STEMIs, the reduction was higher for women (41.2%; P = 0.011) than men (17.8%; P = 0.191). A similar reduction in AMI admissions was registered in North Italy (52.1%), Central Italy (59.3%), and South Italy (52.1%). The STEMI case fatality rate during the pandemic was substantially increased compared with 2019 [risk ratio (RR) = 3.3, 95% CI 1.7–6.6; P < 0.001]. A parallel increase in complications was also registered (RR = 1.8, 95% CI 1.1–2.8; P = 0.009). Conclusion Admissions for AMI were significantly reduced during the COVID-19 pandemic across Italy, with a parallel increase in fatality and complication rates. This constitutes a serious social issue, demanding attention by the scientific and healthcare communities and public regulatory agencies.

Key Words: vascular smooth muscle cells Ⅲ microRNA Ⅲ miR-133 Ⅲ smooth muscle differentiation Ⅲ vascular remodeling V ascular smooth muscle cells (VSMCs) within adult blood vessels proliferate at a very low rate, exhibit very low synthetic activity, and express a unique repertoire of contractile proteins, ion channels, and signaling molecules. 1 Unlike skeletal muscle and cardiac muscle, which consist of terminally differentiated cells, adult VSMCs retain remarkable plasticity and can undergo rather profound and reversible changes in phenotype and growth properties in response to changes in local environmental cues. Salient examples of VSMC plasticity can be seen in response to vascular injury when VSMCs dramatically increase their proliferation, migration, and synthetic capacity, playing a critical role in vascular repair. 1,2 A detrimental consequence of the high degree of plasticity exhibited by adult VSMCs is that it can lead to an adverse phenotypic switch and acquisition of characteristics that can contribute to development or progression of vascular disease in humans, including atherosclerosis, restenosis, cancer, and hypertension. [1][2][3] VSMC phenotypic modulation is characterized by significant changes in gene expression patterns, matrix and cytokine production, contractility, and growth state, ultimately leading to their switch from a synthetic to a proliferative phenotype.Original received January 3, 2011; revision received August 8, 2011; accepted August 9, 2011. In July 2011, the average time from submission to first decision for all original research papers submitted to Circulation Research was 13.5 days.From Thus, understanding the regulatory mechanisms underlying the VSMC phenotypic switch is of paramount importance. [1][2][3] One of the key breakthroughs for the study of gene expression regulation has recently been the discovery of microRNAs (miRNAs or miRs) and their role in gene silencing through mRNA degradation or translational inhibition. 4,5 Increasing evidence indicates that miRNAs regulate key genetic programs in cardiovascular biology, physiology, and disease. 4,5 In particular, miR-21, -143, -145, -221, -222 have all been implicated to play a role in VSMC function and phenotypic plasticity. 6 -11 More recently, 2 articles demonstrated that miR-1 is induced by myocardin overexpression in human SMCs, contributing to myocardin-dependent reduction of human SMC growth in vitro. 12,13 miR-133a-1/miR-1-2 and miR133a-2/miR-1-1 are 2 bicistronic miRNA clusters reported to be specifically expressed in cardiac and skeletal muscle. 4,5 A third bicistronic miRNA cluster, comprising miR-206 and miR-133b, is expressed specifically in skeletal muscle but not in the heart. 4,5 miR-1 (miR-1-1/miR-1-2) and miR-133 (miR133a-1/miR-133a-2) play essential roles in cardiac and skeletal muscle development, physiology, and disease 4,5 ; however, their functions in VSMCs and vascular disease are largely unknown. Thus, the aim of the present study was to evaluate the role, if any, of miR-1 and miR-133 in V...

ObjectivesThis study intends to gain further insights into the natural history, the yield of familial and genetic screening, and the arrhythmogenic mechanisms in the largest cohort of short QT syndrome (SQTS) patients described so far.BackgroundSQTS is a rare genetic disorder associated with life-threatening arrhythmias, and its natural history is incompletely ascertained.MethodsSeventy-three SQTS patients (84% male; age, 26 ± 15 years; corrected QT interval, 329 ± 22 ms) were studied, and 62 were followed for 60 ± 41 months (median, 56 months).ResultsCardiac arrest (CA) was the most frequent presenting symptom (40% of probands; range, <1 month to 41 years). The rate of CA was 4% in the first year of life and 1.3% per year between 20 and 40 years; the probability of a first occurrence of CA by 40 years of age was 41%. Despite the male predominance, female patients had a risk profile superimposable to that of men (p = 0.49). The yield of genetic screening was low (14%), despite familial disease being present in 44% of kindreds. A history of CA was the only predictor of recurrences at follow-up (p < 0.0000001). Two patterns of onset of ventricular fibrillation were observed and were reproducible in patients with multiple occurrences of CA. Arrhythmias occurred mainly at rest.ConclusionsSQTS is highly lethal; CA is often the first manifestation of the disease with a peak incidence in the first year of life. Survivors of CA have a high CA recurrence rate; therefore, implantation of a defibrillator is strongly recommended in this group of patients.

A hyperadrenergic state is a seminal aspect of chronic heart failure. Also, "Takotsubo stress cardiomyopathy," is associated with increased plasma catecholamine levels. The mechanisms of myocyte damage secondary to excess catecholamine exposure as well as the consequence of this neurohumoral burst on cardiac stem cells (CSCs) are unknown. Cardiomyocytes and CSCs were exposed to high doses of isoproterenol (ISO), in vivo and in vitro. Male Wistar rats received a single injection of ISO (5 mg kg؊1 ) and were sacrificed 1, 3, and 6 days later. In comparison with controls, LV function was impaired in rats 1 day after ISO and started to improve at 3 days. The fraction of dead myocytes peaked 1 day after ISO and decreased thereafter. ISO administration resulted in significant ryanodine receptor 2 (RyR2) hyperphosphorylation and RyR2-calstabin dissociation. JTV519, a RyR2 stabilizer, prevented the ISO-induced death of adult myocytes in vitro. In contrast, CSCs were resistant to the acute neurohumoral overload. Indeed, CSCs expressed a decreased and inverted complement of ␤ 1 /␤ 2 -adrenoreceptors and absence of RyR2, which may explain their survival to ISO insult. Thus, a single injection of ISO causes diffuse myocyte death through Ca 2؉ leakage secondary to the acutely dysfunctional RyR2. CSCs are resistant to the noxious effects of an acute hyperadrenergic state and through their activation participate in the response to the ISO-induced myocardial injury. The latter could contribute to the ability of the myocardium to rapidly recover from acute hyperadrenergic damage.

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