Fatal myocardial damage due to zinc phosphide intentional ingestion

We present a case of fatal myocardial damage caused by zinc phosphide ingestion. It is a highly toxic poison that causes life-threatening complications (cardiac and respiratory acute failure above all) by its active metabolite phosphine. Phosphine toxicity's case reports from Europe (and Italy), United States and western countries are rare. A 69-year-old man drunk a great amount of alcohol and unspecified amount of diluted zinc phosphide and was admitted to emergency department with a mild metabolic acidosis and acute respiratory failure. After gastro-intestinal decontamination, a transient improvement of his clinical conditions was observed. In the emergency medicine unit a sudden onset of severe bradycardia and hypotension appeared, electrocardiogram showed an increase in QRS duration with ST elevation in many leads; 2 min later a thirddegree atrio-ventricular block was evident. Bradycardia went into asystole and the patient had cardiac arrest. Despite all resuscitative maneuvers, 6 h after zinc phosphide ingestion the patient died. No antidote or specific therapy or management of this potentially lifethreatening poison are actually available, but only supportive and resuscitative measures

Fatal myocardial damage due to zinc phosphide intentional ingestion

We present a case of fatal myocardial damage caused by zinc phosphide ingestion. It is a highly toxic poison that causes life-threatening complications (cardiac and respiratory acute failure above all) by its active metabolite phosphine. Phosphine toxicity’s case reports from Europe (and Italy), United States and western countries are rare. A 69-year-old man drunk a great amount of alcohol and unspecified amount of diluted zinc phosphide and was admitted to emergency department with a mild metabolic acidosis and acute respiratory failure. After gastro-intestinal decontamination, a transient improvement of his clinical conditions was observed. In the emergency medicine unit a sudden onset of severe bradycardia and hypotension appeared, electrocardiogram showed an increase in QRS duration with ST elevation in many leads; 2 min later a thirddegree atrio-ventricular block was evident. Bradycardia went into asystole and the patient had cardiac arrest. Despite all resuscitative maneuvers, 6 h after zinc phosphide ingestion the patient died. No antidote or specific therapy or management of this potentially lifethreatening poison are actually available, but only supportive and resuscitative measures

Frequency of Left Ventricular Hypertrophy in Non-Valvular Atrial Fibrillation

Left ventricular hypertrophy (LVH) is significantly related to adverse clinical outcomes in patients at high risk of cardiovascular events. In patients with atrial fibrillation (AF), data on LVH, that is, prevalence and determinants, are inconsistent mainly because of different definitions and heterogeneity of study populations. We determined echocardiographic-based LVH prevalence and clinical factors independently associated with its development in a prospective cohort of patients with non-valvular (NV) AF. From the "Atrial Fibrillation Registry for Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study" (ARAPACIS) population, 1,184 patients with NVAF (mean age 72 \ub1 11 years; 56% men) with complete data to define LVH were selected. ARAPACIS is a multicenter, observational, prospective, longitudinal on-going study designed to estimate prevalence of peripheral artery disease in patients with NVAF. We found a high prevalence of LVH (52%) in patients with NVAF. Compared to those without LVH, patients with AF with LVH were older and had a higher prevalence of hypertension, diabetes, and previous myocardial infarction (MI). A higher prevalence of ankle-brachial index 640.90 was seen in patients with LVH (22 vs 17%, p = 0.0392). Patients with LVH were at significantly higher thromboembolic risk, with CHA2DS2-VASc 652 seen in 93% of LVH and in 73% of patients without LVH (p <0.05). Women with LVH had a higher prevalence of concentric hypertrophy than men (46% vs 29%, p = 0.0003). Logistic regression analysis demonstrated that female gender (odds ratio [OR] 2.80, p <0.0001), age (OR 1.03 per year, p <0.001), hypertension (OR 2.30, p <0.001), diabetes (OR 1.62, p = 0.004), and previous MI (OR 1.96, p = 0.001) were independently associated with LVH. In conclusion, patients with NVAF have a high prevalence of LVH, which is related to female gender, older age, hypertension, and previous MI. These patients are at high thromboembolic risk and deserve a holistic approach to cardiovascular prevention