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Purpose: Previous research identified decreased overall and cardiovascular mortality for National Football League (NFL) players from the 1959-1988 era. The present study explored the mortality risk among recent NFL players who played in an era of heavier linemen and nearly year-round physical conditioning., Methods: This cohort study included 9778 former NFL players with at least 1 yr in the NFL whose last season was between 1986 and 2012. Players' pension fund records were matched to the National Death Index to determine vital status, date of death, and cause of death. Standardized mortality ratios (SMR) compared player mortality through 2014 with US men of the same age, race, and calendar year. Cox proportional hazards models assessed the effect of player characteristics on overall and cardiovascular mortality., Results: Two percent (n = 227) of players were deceased, with a median age at death of 38 yr (range, 23-61 yr). The most common major causes of death were diseases of the heart (n = 47; 21%), violence (n = 39; 17%), and transportation injuries (n = 34; 15%). Risk of death was significantly lower than the general population for overall mortality (SMR, 0.46, 95% confidence interval (CI), 0.40-0.52), cardiovascular disease (SMR, 0.65; 95% CI, 0.50-0.84), and other major causes. Players with playing-time body mass index (BMI) of >35 kg·m had significantly higher cardiovascular disease mortality (SMR, 2.20; 95% CI, 1.32-3.44) than did the general population and higher overall mortality risk (standardized rate ratio, 3.84; 95% CI, 2.66-5.54) than did players with a BMI of <30 kg·m., Conclusions: Consistent with an earlier NFL cohort and other elite athlete populations, the overall and cardiovascular mortality risk of this NFL cohort was significantly lower than that of the general US male population, likely attributable to a healthy worker effect and less smoking.However, players with the highest playing-time BMI exhibited elevated cardiovascular mortality risk.

Background: Controversy exists regarding the use of magnesium in the treatment of acute myocardial infarction (AMI) because of apparent conflicting results from clinical trials. One hypothesis to explain the various clinical observations proposes that the timing of magnesium administration significantly influences its therapeutic effect; ie, supraphysiological levels of Mg2+ must be present at the time of reperfusion for magnesium to produce clinical benefit., Methods and Results: These experiments evaluated the effect of varying the timing of magnesium administration during AMI. Female Yorkshire swine (34 to 42 kg) underwent thoracotomy and 50 minutes of left anterior descending coronary artery (LAD) occlusion, followed by 3 hours of reperfusion. In the first group, MgSO4 (250 mg of magnesium diluted in 60 cm3 saline) was infused into the LAD over 12 minutes, beginning immediately with the onset of reperfusion (n = 6, Mg-early group). In the second group, MgSO4 was given after 1 hour of reperfusion (n = 6, Mg-late group). Six pigs received saline instead of magnesium and served as the control group. Lethal arrhythmias were significantly reduced in the Mg-early group. Infarct size was determined by vital staining. Infarct size was 0.16 +/- 0.05 g/kg body wt (Mg-early), 0.35 +/- 0.08 g/kg (Mg-late), and 0.42 +/- 0.04 g/kg for the control group. Compared with the control group, significant (P = .029) reduction in infarct size occurred in the Mg-early group but not in the Mg-late group., Conclusions: We conclude that intracoronary MgSO4 delivered during reperfusion can significantly diminish infarct size in swine, but the timing of administration is critical.

Background: Practitioners often assume a close relation between angiographic coronary artery stenosis and patient functional capacity. To test this unproven hypothesis, we analyzed the relation between coronary artery stenosis measured by different methods and maximal treadmill exercise tolerance in patients with single-vessel disease before and after intervention by percutaneous transluminal coronary angioplasty (PTCA)., Methods and Results: Coronary angiography and maximal exercise testing off anti-ischemic medication were performed before random assignment of 227 patients with single-vessel coronary artery disease to PTCA or drug therapy. Six months later, angiography and exercise testing were repeated with patients assigned to PTCA off anti-ischemic therapy so that the altered coronary stenosis was the only consistent variable. Patients assigned to drug therapy were exercised on drug therapy. Coronary stenosis was assessed visually by the local investigator and quantitatively by blinded caliper and computer methods in central laboratories. Variabilities of caliper and computer measurements were established in a subset read twice. Visually estimated stenosis > or = 90% at baseline was associated with shorter exercise duration (7.9 versus 9.2 minutes, P < .04). Similar segregation at baseline was not observed with caliper or computer methods. Regardless of the method of measurement used, correlation between changes of lesion severity and exercise duration from baseline to follow-up was poor. Patients were angiographically classified as "better," "unchanged," or "worse" if follow-up stenosis was below, within, or above 2 SD of mean technical variability from baseline (+/- 18.8%, caliper, +/- 14.6%, computer). Exercise duration for PTCA patients improved among those with better lesions (+2.4 minutes, n = 50, P = .001) but also among those with unchanged lesions (+1.9 minutes, n = 41, P < or = .001). Unchanged medically treated patients improved less (+0.5 minutes, n = 86, P = .04). Results were similar when patients were angiographically classified by minimum lumen diameter., Conclusions: Handheld calipers and quantitative coronary angiography are equivalent techniques for making anatomic measurements. Neither method identified patients having reduced exercise capacity at baseline as well as visual estimation. The relation between changes of coronary stenosis and exercise duration is highly variable, at least in part because of the insensitivity of angiographic methods for detecting small but potentially important changes. Minimal anatomic improvement 6 months after PTCA does not preclude a good functional outcome. Contrary to common belief, angiographic stenosis does not correlate well with functional capacity, even in patients with single-vessel disease.

To evaluate the relative long-term improvement in coronary artery hemodynamics after revascularization by coronary artery bypass graft surgery (CABG) or percutaneous transluminal coronary angioplasty (PTCA), regional coronary flow reserve (CFR) was measured, by digital computer analysis of 35 mm cine film, in 50 men undergoing cardiac catheterization. CFR (mean +/- SEM) in 12 atherosclerotic arteries before revascularization was 1.02 +/- 0.05. Mean CFR in 29 normal arteries of men with normal coronary arteriograms was significantly higher (2.59 +/- 0.11) than that in 16 atherosclerotic arteries of patients revascularized by CABG (2.02 +/- 0.17, p less than .01) or in 14 atherosclerotic arteries of those revascularized by PTCA (1.97 +/- 0.12, p less than .01). No difference in CFR between the CABG and PTCA groups was found and variables known to influence CFR were similar between groups. Equivalent and significant long-term improvement in coronary artery hemodynamics is provided by CABG or PTCA. We postulate that the difference in CFR in the men with normal arteries and those who underwent revascularization was related to the effects of the general atherosclerotic process, which remain despite successful treatment by these techniques.

A technique was developed for measuring regional myocardial perfusion by intracoronary infusions of hydrogen (H2)-saturated saline. H2 concentration was detected during washout in the pulmonary artery by means of the voltage response of a platinum-tipped electrode. Regional myocardial perfusion was calculated from the H2 exponential desaturation curve according to the Kety-Schmidt principle. In 16 anesthetized open-chest dogs, validation of this technique was performed at baseline, reduced (stenosis), and hyperemic (dipyridamole) flow states by means of the radionuclide-labeled microsphere reference withdrawal technique. There was an excellent quadratic correlation between microsphere and H2 washout techniques (range 0.11 to 3.15 ml/min/g) (n = 33, r = .92, y = -0.12x2 + 0.89x + 0.20, SEE = 0.20 ml/min/g; p less than .0001). Hyperemic regional myocardial perfusion was underestimated by H2 washout and severely ischemic regional myocardial perfusion was overestimated. When regional myocardial perfusion values greater than twice normal were excluded, a strong linear correlation was present between H2 and microsphere measurements (n = 27, r = .89, y = 0.76x + 0.22, SEE = 0.18 ml/min/g; p less than .0001). The H2 washout method was further tested in 18 additional open chest dogs for calculations of the mass of an arterial perfusion bed according to the principle that the mass of the bed (g) equals coronary blood flow (ml/min) divided by regional myocardial perfusion (ml/min/g).(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the effect of angioplasty-induced arterial injury on regional coronary blood flow, resting and postocclusion reactive hyperemic flows were measured in the left anterior descending (LAD) and circumflex (LCx) coronary arteries of 32 dogs after one of four interventions in the LAD with a balloon angioplasty catheter: group A, no injury; group B, endothelial denudation; group C, medial injury; group D, pretreatment with 325 mg of aspirin 2 hr before medial injury. Resting flows did not change in any group. In group C, hyperemic flow decreased in both the LAD and LCx by 15% to 20% (p less than .001) over 30 to 90 min, suggesting that a circulating substance changed coronary resistance. Histologic and ultrastructural studies of the LADs demonstrated an intact endothelial cell layer in group A, endothelial disruption with a few adherent platelets in group B, medial injury with a dense layer of adherent platelets in group C, and medial injury with a few adherent platelets in group D. Thus endothelial denudation results in relatively mild platelet deposition and no change in resting or hyperemic coronary blood flow. In contrast, medial injury results in relatively marked platelet deposition and a significant decrease in hyperemic flow, both of which are prevented by platelet inhibition with aspirin.

To assess potential differences in the intrinsic properties of image recording media and their impact on quantitative coronary arteriography, we used an automatic quantitative arteriography computer program to analyze cine film and digital radiographic images of a radiographic arterial phantom. The phantom consisted of a lucite plate with precision-drilled lumena ranging from 0.5 to 5.0 mm in diameter. Film images were digitized at 2048 X 2048 pixel resolution, and digital radiographic images were acquired at 512 X 512 and 1024 X 1024 resolution. Arterial geometric diameter, percent diameter stenosis, densitometric relative cross-sectional area, and densitometric percent area stenosis were measured. All three techniques were equivalent in measuring diameters with a high degree of overall accuracy (R greater than .992). All methods overestimated diameters below 1.0 mm. Both 512 X 512 and 1024 X 1024 digital images were superior to film for densitometric measurement of relative area (R = .995 vs. R = .940, P = .0032). We conclude that automated analysis of digital radiographic images yields results that are similar in geometric precision but greater in densitometric precision than film analysis.

Quantitative coronary arteriography has been shown to be useful in assessing the extent of coronary disease, its functional significance, and its response to therapeutic interventions. Most current methods rely either on hand-drawn arterial contours or automatic edge-detection algorithms applied to 35 mm cineangiograms. To assess the performance in vivo of a new, fully automatic, rapid coronary quantitation program, dogs were instrumented with precision-drilled, plastic cylinders to create intraluminal stenoses in the left anterior descending and/or circumflex arteries, as well as with high-fidelity micromanometers and electromagnetic flow probes. Stenosis diameters ranged from 0.83 to 1.83 mm. Biplane, on-line, digital coronary angiograms and cineangiograms were recorded during standard selective coronary arteriography in the closed-chest preparation. The on-line digital images were analyzed in nonsubtracted and subtracted modes. Cineangiograms were digitized to allow coronary quantitation by the same computer program. There was an excellent correlation between known and measured minimal diameter stenoses (r = .87 to .98, SEE = 0.09 to 0.24 mm). Interobserver and intraobserver variability analysis showed high reproducibility (r = .90 to .97, SEE = 0.12 to 0.23 mm). The best results in both analyses were achieved by nonsubtracted digital imaging and the worst by cineradiography. Measures of percent diameter stenosis, percent area stenosis (geometric and videometric), and absolute minimal cross-sectional area (geometric and videometric) were all significantly correlated with independent measures of actual coronary flow reserve. This study provides direct anatomic and physiologic validation in vivo of a new and rapid coronary quantitation method suitable for analysis of both digital angiograms and cineangiograms.

With current interest in digital and densitometric angiographic techniques for evaluating coronary blood flow (CBF), the immediate effects of intracoronary contrast injections on CBF are important to establish. We investigated the effects of ECG-gated intracoronary injection of contrast on CBF with different injection rates (1-6 cc/sec), volumes (1/2-6 cc), and contrast concentrations (1/2, full strength). Sixteen open-chest dogs were instrumented with electromagnetic flow probes on the left anterior descending artery. During intracoronary injections of contrast, a characteristic decrease in coronary blood flow to approximately 45% of preinjection levels was seen an average of 1.9 seconds after intracoronary contrast injection. The timing of the depression in coronary flow was most influenced by the rate of contrast injection, and the magnitude of depression in flow was influenced by both the volume and concentration of the contrast injection. Angiographic techniques using the first 6 seconds after injection to obtain CBF measurements should take these characteristic changes into account to avoid possible errors.