Large lungs in divers: natural selection or a training effect?

BACKGROUND: Normal spirometry is required for medical clearance of professional divers in many countries. Divers frequently have unusually large lung volumes associated with a low ratio of FEV(1) to FVC (FEV(1)%), suggestive of obstructive airways disease. We retrospectively analyzed the records of divers in the Israeli Navy with a low FEV(1)% who fulfilled the criteria for large lungs, to determine whether this might be the effect of training or natural selection. We also investigated changes in pulmonary function in relation to diving experience. METHODS: A total of 171 divers with FEV(1)% < 80% on simple spirometry were evaluated. We conducted a retrospective analysis of lung function data for those subjects who met the criteria for large lungs. RESULTS: One hundred nine of 171 divers with low FEV(1)% met the criteria for large lungs and were included in the study. Their average age was 25 years (range, 18 to 44 years), and their mean diving experience was 7 years (range, 0 to 26 years). No difference was found in FVC values between experienced and inexperienced divers. The mean forced expiratory flow at 50% of vital capacity was significantly reduced in the most experienced group compared with the novice or less experienced divers. No difference was found in the diffusing capacity of the lung for carbon monoxide between experienced and inexperienced divers. CONCLUSIONS: We suggest that large lungs may represent part of the natural selection for diving, rather than a training effect. Prolonged diving experience may result in the development of small airways disease.     

Simvastatin-induced myocardial protection against ischemia-reperfusion injury is mediated by activation of ATP-sensitive K+ channels

OBJECTIVES: Previous studies have suggested that the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors attenuate ischemia-reperfusion injury. We investigated whether pretreatment with simvastatin reduces myocardial infarct size and whether glyburide, a non-selective inhibitor of the ATP-sensitive K channels, abrogates this infarct size-limiting effect. METHODS: Sprague-Dawley rats were treated with either simvastatin (20 mg/kg per day) or saline alone for 3 days. Additional groups of rats were treated as above and on the fourth day they received intravenous glyburide (0.3 mg/kg). All rats underwent 30 min of coronary artery occlusion followed by 180 min of reperfusion. Ischemic myocardium at risk was assessed with blue dye and infarct size with triphenyltetrazolium chloride. RESULTS: Infarct size, expressed as a percentage of the myocardium at risk, was significantly smaller in the simvastatin group (n = 8, 20.8 +/- 3.4%) than in the placebo group (n = 6, 40.1 +/- 2.7%) (P = 0.001). Glyburide abolished the protective effect of simvastatin with infarct size being 34.2 +/- 6.9% and 29.7 +/- 3.9% of the area at risk in the simvastatin group (n = 7) and placebo (n = 7) group, respectively (P = 0.58). CONCLUSIONS: Simvastatin significantly reduced myocardial infarct size. The protective effect was completely abrogated by glyburide, strongly suggesting that this protective effect is mediated via activation of the ATP-sensitive K channels.     

Ticagrelor and Dapagliflozin Have Additive Effects in Ameliorating Diabetic Nephropathy in Mice with Type-2 Diabetes Mellitus

Cardiovascular Drugs and Therapy - Ticagrelor and dapagliflozin can suppress the activation of the NOD-like receptor 3 (NLRP3)-inflammasome and activate AMP-activated protein kinase (AMPK). The...     

Plasma homocysteine, methylenetetrahydrofolate reductase genotypes, and age at onset of symptoms of myocardial ischemia

Elevated fasting plasma homocysteine is a graded risk factor of coronary artery disease (CAD) and may accelerate onset of CAD. Homozygosity for the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is commonly but inconsistently associated with hyperhomocysteinemia. In the present study we examined the possible relation between levels of fasting plasma homocysteine and age at CAD onset in different MTHFR genotypes. We studied 182 patients with CAD, 74 patients with early onset CAD (aged < or = 45 years), and 108 patients with later onset CAD (aged 46 to 65 years). Plasma homocysteine levels in 90 subjects without CAD were used for control. Fasting plasma homocysteine levels in T/T homozygotes with early onset CAD (20.2 +/-12.5 micromol/L) was markedly higher than in T/T homozygotes with later onset CAD (13.4 +/- 6.8 micromol/L) and in patients with early onset CAD who were not T/T homozygotes (11.9 +/- 3.7 micromol/L; p = 0.034 and p = 0.0001, respectively). CAD developed earlier in T/T homozygotes who were hyperhomocysteinemic (>15 micromol/L) than in the T/T homozygotes who were not (p = 0.036). Plasma homocysteine levels had no effect on age at onset of CAD in patients who were non-T/T genotypes. Homocysteine levels in control subjects and in patients who were non-T/T genotypes were comparable and were not influenced by age. The results reveal an inverse relation between the level of fasting plasma homocysteine and age at onset of CAD in T/T homozygotes as opposed to no association in patients who were non-T/T genotypes. Additionally, these results show that hyperhomocysteinemia and the T/T genotype have a stronger effect on the pathogenesis of CAD when they are combined, and that a marked increase (>15 micromol/L) in fasting plasma homocysteine in T/T homozygotes is a risk factor for early onset of CAD.     

Acute anterior wall myocardial infarction entailing st-segment elevation in lead v1: Electrocardiographic and angiographic correlations

Background: The correlation between ST elevation in lead V₁ during anterior wall acute myocardial infaction (AMI) and the culprit lesion site in the left anterior descending (LAD) coronary artery is poor. Hypothesis: The study was undertaken to assess the electrocardiographic (ECG) characteristics and angiographic significance of ST-segment elevation in lead V¹ during anterior wall acute myocardial infarction (AMI). Methods: Data from 115 patients with anterior wall AMI, who underwent coronary angiography within 14 days of hospitalization, were studied. The admission 12-lead ECG was examined and the coronary angiogram was evaluated for the nature of the conal branch of the right coronary artery (RCA) and for the culprit lesion site in the left anterior descending (LAD) coronary artery. Results: Mean ST-segment deviation and the frequency of patients with ST-segment elevation > 0.1 mV were significantly lower in lead V i than in lead V2 (0.136 $$ 0.111 mV vs. 0.421 $$ 0.260 mV, and 37 vs. 96%, for leads Vi and Vi, respectively). A small conal branch not reaching the interventricular septum (IVS) was more prevalent among patients with ST-segnicni elevation >0.1 mV in lead Vi (67%), whereas a large conal branch was more prevalent in patients with ST-segment deviation (1 mV in that lead (83%, p<0.001). No relation was found between ST-segment deviation in lead V i during anterior wall AMI and the culprit lesion site in the LAD. Conclusion: ST-segment elevation in lead V₁ during first anterior wall AMI was found in one third of the patients, and its magnitude was lower than that in the other precordial leads. ST-segment elevation in lead V₁ favors the presence of a small conal branch of the RCA that does not reach the IVS.     

A counterpoint paper: Comments on the electrocardiographic part of the 2018 Fourth Universal Definition of Myocardial Infarction endorsed by the International Society of Electrocardiology and the International Society for Holter and Noninvasive Electrocardiology

The Fourth Universal Definition of Myocardial Infarction (FUDMI) focuses on the distinction between nonischemic myocardial injury and myocardial infarction (MI), along with the role of cardiovascular magnetic resonance, in order to define the etiology of myocardial injury. As a consequence, there is less emphasis on updating the parts of the definition concerning the electrocardiographic (ECG) changes related to MI. Evidence of myocardial ischemia is a prerequisite for the diagnosis of MI, and the ECG is the main available tool for (a) detecting acute ischemia, (b) triage, and (c) risk stratification upon presentation. This review focuses on multiple aspects of ECG interpretation that we firmly believe should be considered for incorporation in any future update to the Universal Definition of MI.     

Updated Electrocardiographic Classification of Acute Coronary Syndromes

The electrocardiogram (ECG) findings in acute coronary syndrome should always be interpreted in the context of the clinical findings and symptoms of the patient, when these data are available. It is important to acknowledge the dynamic nature of ECG changes in acute coronary syndrome. The ECG pattern changes over time and may be different if recorded when the patient is symptomatic or after symptoms have resolved. Temporal changes are most striking in cases of ST-elevation myocardial infarction. With the emerging concept of acute reperfusion therapy, the concept ST-elevation/non-ST elevation has replaced the traditional division into Q-wave/non-Q wave in the classification of acute coronary syndrome in the acute phase.

Keypoints:

In acute coronary syndrome, in addition to the traditional electrocardiographic risk markers, such as ST depression, the 12-lead ECG contains additional, important diagnostic and prognostic information. Clinical guidelines need to acknowledge certain high-risk ECG patterns to improve patient care.