The association between heavy metal and serum cholesterol levels in the US population: National Health and Nutrition Examination Survey 2009-2012.

BACKGROUND: Few studies have examined the relationship between heavy metal and serum cholesterol levels, and no recent study has examined this relationship in the US population. METHODS AND RESULTS: A total of 19,591 individuals aged 0-80 years were included in the National Health and Nutrition Examination Survey 2009-2012; the current study was composed of survey participants for whom some or all low-density lipoprotein cholesterol (LDL-C), serum triglyceride, high-density lipoprotein cholesterol, total cholesterol, blood lead (Pb), total blood mercury (Hg), and blood cadmium (Cd) levels had been measured. Three tertiles (T1-T3) of heavy metals were used to explore dose-response association between heavy metal exposure and serum cholesterol level. Logistic regression was used to explore the relationship between tertiles of blood heavy metal levels and serum cholesterol levels after adjusting for age, sex, and socioeconomic status. We have shown that the groups with the highest levels of Pb, Hg, and Cd had a 56%, 73%, and 41% chance, respectively, of having a high total cholesterol level. In study subjects with the highest Pb levels, there was also a 22% chance of being in the group with the highest LDL-C level. An increase in total cholesterol and LDL-C levels was observed from the first to the third tertiles of the heavy metals studied. CONCLUSION: Increasing blood Pb, Hg, and Cd levels were associated with significantly increased odds of high total cholesterol after adjusting for age, sex, and socioeconomic status.

The C of CHADS: Historical perspective and clinical applications for anticoagulation in patients with non valvular atrial fibrillation and congestive heart failure.

The risk stratification of patients with coexisting non valvular atrial fibrillation and congestive heart failure, is often a clinical challenge, as the definitions of congestive heart failure in the popular CHADS2 and CHA2DS2VASc scoring systems, and amongst major clinical trials on Warfarin and Novel Oral Anticoagulants (NOAC) have heterogeneity. Available evidence reveals that any heart failure and/or left ventricular systolic dysfunction is associated with higher rates of stroke/systemic embolism and bleeding in patients with non valvular atrial fibrillation compared to patients without heart failure and normal left ventricular function. Most standard dose NOAC regimens have a better safety and efficacy profile over warfarin in most heart failure sub-group types with a few exceptions including patients with NYHA III/IV on Dabigatran 150mg BID from the RE-LY trial, who had higher major bleeding events, and patients with asymptomatic left ventricular dysfunction (ejection fraction ≤40%) and heart failure with reduced ejection fraction on 20mg of Rivaroxaban in the ROCKET-AF trial, when compared to patients on Warfarin in the corresponding groups. With the gaining popularity and use of NOACs, understanding their safety profile in such situations is paramount.

Origin of the giant R wave in acute transmural myocardial infarction in the pig.

An increase in R wave amplitude and a diminution of S wave amplitude, together with ST segment elevation, have been described as very early electrocardiographic changes during clinical and experimental acute myocardial infarction. The genesis of these QRS changes remains unclear. We assessed the quantitative relationship between the local conduction delay and the formation of the giant R wave, using multiple epicardial, intramural unipolar, and bipolar electrodes in 30 open-chest pigs with acute transmural myocardial ischemia. Blood pressure, heart rate, serum electrolytes, hematocrit, and left ventricular size remained constant, or varied insignificantly throughout the experiments. In nonischemic pigs, transmural left ventricular activation occurred nearly simultaneously, and the activation time was not correlated with the net QRS potential. During acute ischemia, a giant R wave developed at all of the electrodes located within the ischemia region; R wave amplitude began to increase 1 min after coronary artery ligation (p less than 0.05), compared to control amplitude and peaked at 8 min (p less than 0.0001). The degree of conduction delay at a given site was correlated linearly with the local R wave amplitude (average of correlation coefficients +/- SEM at 1 min, r = 0.64 +/- 0.08, and at 8 min, r = 0.81 +/- 0.06). The magnitude of the R wave potential and the conduction delay were greater in regions deep inside the ischemic zone than in the border and normal areas (p less than 0.0001), and were greater in subepicardial than in subendocardial areas (p less than 0.05). In summary, during transmural ischemia, conduction is markedly slowed, and an orderly and discrete wavefront advances toward the center of the ischemic zone from lateral and subendocardial areas. When depolarization is complete in the rest of the heart, this slow activation front becomes temporally isolated and its progression gives rise to a giant R wave, which appears in recordings from overlying electrodes.

Rapid expansion of a saccular aneurysm on the left coronary sinus of Valsalva: a role for early surgical repair?

A thirty nine year old woman presented with ischaemic chest pain caused by a saccular aneurysm of the left coronary sinus of Valsalva. Over the next two weeks there was rapid dilatation of the aneurysm which led to left coronary artery compression and death from a massive myocardial infarction. It is suggested that early repair should be considered in patients with saccular aneurysm at this site, but only in the context of other management priorities.

The giant R wave of acute myocardial infarction.

The common clinical electrocardiographic criteria for diagnosis of acute transmural myocardial infarction include ST segment elevation and tall, upright T waves, but do not include changes in QRS morphology. The purpose of this study was to show that development of a 50% or greater increase in R wave amplitude, the giant R wave, in patients with acute transmural myocardial infarction occurs, and also to characterize changes in QRS morphology which may aid the ECG diagnosis of acute transmural myocardial infarction. Over the past 6 years, 36 patients with an increase in R wave amplitude during acute transmural myocardial infarction were identified at the Strong Memorial Hospital Coronary Care Unit. A significant increase in R wave height (0.33 +/- 0.10 to 0.97 +/- 0.08 mV, p less than 0.05), width (0.03 +/- 0.00 to 0.08 +/- 0.01, p less than 0.05) and area (0.01 +/- 0.00 to 0.05 +/- 0.01 mV-msec, p less than 0.05) appeared in the same ECG lead demonstrating ST segment elevation and tall T waves during the acute phase of transmural myocardial infarction. Patients with diaphragmatic myocardial infarction showed a significant (p less than 0.05) rightward QRS frontal plane axis shift and patients with anterior wall myocardial infarctions developed an anterior QRS axis shift in the horizontal plane during occurrence of the giant R wave. We conclude from this preliminary study that the giant R wave may be observed during acute transmural myocardial infarction and may in part be caused by local intramyocardial conduction delay in acutely ischemic tissue as supported by an increase in the R wave width along with shifts in the frontal and horizontal plane QRS axis toward the area of acute ischemia. The giant R wave occurs in conjunction with ST segment elevation and tall T waves and may aid the ECG diagnosis of acute transmural myocardial infarction.

Reactions to intravenous contrast media. Part I: Severe and fatal cardiovascular reactions in a canine dehydration model.

Investigations into the nature of severe and fatal reactions to contrast media have been severely limited by their unpredictable occurrence in the clinical setting and the absence of suitable laboratory models. The authors report their experience with a canine dehydration model. Intravenous administration of 2 ml/kg of 76% sodium methylglucamine diatrizoate resulted in vomiting, shock, inappropriate slowing of the heart rate, and death. ECG findings indicated suppression of sinoatrial node automaticity, a decrease in the rate of atrioventricular conduction, and depression of myocardial contractility. These results suggest two possible mechanisms: (a) enhanced vagal tone as the result of stimulation of the vasomotor center of the medulla or (b) accentuation of direct contrast-induced myocardial toxicity.