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1.
Int J Cardiol ; 385: 1-7, 2023 08 15.
Article in English | MEDLINE | ID: mdl-37211051

ABSTRACT

BACKGROUND: Spontaneous coronary artery dissection (SCAD) often presents with acute coronary syndrome and underlying pathophysiology involves the interplay between predisposing factors and precipitating stressors, such as emotional and physical triggers. In our study we sought to compare clinical, angiographic and prognostic features in a cohort of patients with SCAD according to the presence and type of precipitating stressors. METHODS: Consecutive patients with angiographic evidence of SCAD were divided into three groups: patients with emotional stressors, patients with physical stressors and those without any stressor. Clinical, laboratoristic and angiographic features were collected for each patient. The incidence of major adverse cardiovascular events, recurrent SCAD and recurrent angina was assessed at follow-up. RESULTS: Among the total population (64 subjects), 41 [64.0%] patients presented with precipitating stressors, including emotional triggers (31 [48.4%] subjects) and physical efforts (10 [15.6%] subjects). As compared with the other groups, patients with emotional triggers were more frequently female (p = 0.009), had a lower prevalence of hypertension (p = 0.039] and dyslipidemia (p = 0.039), were more likely to suffer from chronic stress (p = 0.022) and presented with higher levels of C-reactive protein (p = 0.037) and circulating eosinophils cells (p = 0.012). At a median follow-up of 21 [7; 44] months, patients with emotional stressors experienced higher prevalence of recurrent angina (p = 0.025), as compared to the other groups. CONCLUSIONS: Our study shows that emotional stressors leading to SCAD may identify a SCAD subtype with specific features and a trend towards a worse clinical outcome.


Subject(s)
Coronary Vessel Anomalies , Vascular Diseases , Humans , Female , Prognosis , Coronary Vessels , Precipitating Factors , Vascular Diseases/epidemiology , Coronary Vessel Anomalies/epidemiology , Angina Pectoris , Coronary Angiography/adverse effects , Risk Factors
2.
G Ital Cardiol (Rome) ; 21(6): 417-420, 2020 Jun.
Article in Italian | MEDLINE | ID: mdl-32425184

ABSTRACT

Takotsubo syndrome (TTS) is one of the causes of myocardial infarction with non-obstructive coronary arteries, and is often triggered by physical events (e.g. acute respiratory failure), or emotional events (e.g. loss of a family member, cardiac stress induced by an acute illness). SARS-CoV-2 pneumonia currently represents a worldwide health problem; the correlations between cardiovascular disease, myocardial injury and SARS-CoV-2 infection are still unclear, but initial data show that myocardial damage represents a negative prognostic factor. Myocardial injury during SARS-CoV-2, as defined by a pathological rise in circulating troponin levels, is not an uncommon complication in hospitalized patients, and is significantly more frequent in intensive care unit patients and among those who died. In this setting, myocardial injury is mainly secondary to type 2 myocardial infarction (mismatch in myocardial oxygen supply and demand during respiratory failure); other causes include myocarditis, coronary thrombosis, sepsis or septic shock. At present, only few cases of TTS have been described during SARS-CoV-2. Here we report the case of a patient hospitalized for pneumonia and respiratory failure due to SARS-CoV-2 with subsequent onset of TTS triggered by both physical and emotional events.


Subject(s)
Betacoronavirus/pathogenicity , Coronavirus Infections/complications , Myocardial Infarction/etiology , Pneumonia, Viral/complications , Takotsubo Cardiomyopathy/etiology , Betacoronavirus/isolation & purification , COVID-19 , Female , Humans , Middle Aged , Myocardial Infarction/virology , Pandemics , Prognosis , SARS-CoV-2 , Takotsubo Cardiomyopathy/virology
3.
G Ital Cardiol (Rome) ; 13(6): 386-95, 2012 Jun.
Article in Italian | MEDLINE | ID: mdl-22622116

ABSTRACT

More women die every year from cardiovascular disease than men from any other cause. Several fundamental variations have been reported in the mechanisms underlying coronary artery disease, which suggest that its genetic basis varies by gender. Such differences are not limited to gonadal hormones and can be seen in the physiology of atherosclerosis, including plaque components, endothelial function and hemostasis. It is possible to speculate that genetic factors are different in men and women and probably involve biological pathways that have not yet been identified. To date, studies performed by means of the candidate gene approach have identified several genetic variants associated with coronary artery disease in women. However, these scientific data have not been translated into clinical practice. It has recently become possible to search for common gene variants that affect the susceptibility to myocardial infarction on the basis of our knowledge of common single nucleotide polymorphisms and haplotypes across the human genome using genome-wide genotyping technologies. Currently more than 20 gene regions have been associated with ischemic heart disease using this approach. However, so far we do not know several genetic variants differently associated with risk of ischemic heart disease in men and women. A challenge for the near future will therefore be to identify genetic variants that maximally differentiate males from females, and also to identify possible relationships between genes and environment and genes and hormones in both sexes.


Subject(s)
Myocardial Ischemia/genetics , Coronary Artery Disease/genetics , Female , Genetic Predisposition to Disease , Humans , Italy/epidemiology , Male , Myocardial Ischemia/mortality , Polymorphism, Genetic , Polymorphism, Single Nucleotide , Prognosis , Risk Factors , Sex Distribution
4.
G Ital Cardiol (Rome) ; 12(10): 686-9, 2011 Oct.
Article in Italian | MEDLINE | ID: mdl-21947114

ABSTRACT

The antiplatelet agent clopidogrel is an effective drug for the prevention of thrombotic events in patients with acute coronary syndrome and in those undergoing percutaneous coronary intervention with the deployment of a coronary stent. However, it has been reported that, despite adequate treatment, about 30% of patients continue to show the high degree of platelet reactivity that is central to the development of atherothrombotic complications and poorer clinical outcomes. Up to 13% of those taking clopidogrel experience a recurrent ischemic event during the first year after acute coronary syndrome, 1-3% experience subacute stent thrombosis after percutaneous coronary intervention probably due to a poor drug response, and about 1.5% experience major bleeding mainly due to an enhanced response. Recent research findings have highlighted the role of genetic variations in determining antiplatelet response variability, and this has aroused interest in genotyping all thienopyridine-eligible patients in order to identify those who would be at increased risk of harm if treated with clopidogrel. However, it remains to be determined whether this information is necessary or sufficient for risk stratification. Only when there are clinical data to support the hypothesis that genotype-guided therapy reduces the rate of ischemic and bleeding events will it be possible to justify the use of genetic testing in all potential patients. When that happens, genotype-guided antiplatelet therapy will also be available in the field of cardiovascular medicine.


Subject(s)
Acute Coronary Syndrome/therapy , Drug-Eluting Stents , Genetic Testing , Platelet Aggregation Inhibitors/therapeutic use , Polymorphism, Genetic , Ticlopidine/analogs & derivatives , Acute Coronary Syndrome/drug therapy , Aged, 80 and over , Angioplasty, Balloon, Coronary/adverse effects , Angioplasty, Balloon, Coronary/methods , Clopidogrel , Genotype , Humans , Male , Platelet Aggregation Inhibitors/administration & dosage , Platelet Aggregation Inhibitors/adverse effects , Practice Patterns, Physicians' , Predictive Value of Tests , Risk Assessment , Thrombosis/etiology , Thrombosis/prevention & control , Ticlopidine/administration & dosage , Ticlopidine/adverse effects , Ticlopidine/therapeutic use , Treatment Outcome
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