Predictors for limb loss among patient with diabetic foot infections: an observational retrospective multicentric study in Turkey.

We aimed to investigate the predictors for limb loss among patients with diabetes who have complicated skin/soft-tissue infections. In this observational study, consecutive patients with diabetic foot infection (DFI) from 17 centres in Turkey, between May 2011 and May 2013 were included. The Turkish DFI Working Group performed the study. Predictors of limb loss were investigated by multivariate analysis. In total, 455 patients with DFI were included. Median age was 61 years, 68% were male, 65% of the patients were hospitalized, 52% of the patients had used antibiotics within the last month, and 121 (27%) had osteomyelitis. Of the 208 microorganisms isolated, 92 (44.2%) were Gram-positive cocci and 114 (54.8%) were Gram-negative rods (GNR). The most common GNR was Pseudomonas; the second was Escherichia coli, with extended spectrum ß-lactamase positivity of 33%. Methicillin-resistant Staphylococcus species were found in 14% (29/208). Amputations were performed in 126/455 (28%) patients, 44/126 (34%) of these were major amputations. In multivariate analysis, significant predictors for limb loss were, male gender (OR 1.75, 95% CI 1.04-2.96, p 0.034), duration of diabetes >20 years (OR 1.9, 95% CI 1.18-3.11, p 0.008), infected ulcer versus cellulitis (OR 1.9, 95% CI 1.11-3.18, p 0.019), history of peripheral vascular disease (OR 2, 95% CI 1.26-3.27, p 0.004), retinopathy (OR 2.25, 95% CI 1.19-4.25, p 0.012), erythrocyte sedimentation rate >70 mm/hr (OR 1.6, 95% CI 1.01-2.68, p 0.05), and infection with GNR (OR 1.8, 95% CI 1.08-3.02, p 0.02). Multivariate analysis revealed that, besides the known risk factors such as male gender, duration of diabetes >20 years, infected ulcers, history of peripheral vascular disease and retinopathy, detection of GNR was a significant predictor of limb loss.

Correlation of coronary with peripheral arterial stenosis. The POSCH Group.

Although it is known that patients with peripheral arterial disease are at high risk for coronary arterial stenosis, it is not known if, conversely, coronary artery disease correlates with peripheral arterial stenosis. In the Program on Surgical Control of the Hyperlipidemias (POSCH) coronary and aortic-iliac-femoral arteriograms were systematically analyzed. POSCH is a randomised, controlled secondary intervention clinical trial of hyperlipidemic subjects, ages 30-64 years with one myocardial infarction and angiographically demonstrable coronary arterial stenosis. Of the 838 subjects enrolled in the study, 436 had diagnostic visualization of both the coronary and aortic-iliac-femoral systems. The aortic-iliac-femoral arteries were normal in 44% (194/436) of the subjects. In contrast, only 9% (37/436) of the subjects had less than 50% stenosis of all 3 coronary arteries. However, there was a positive correlation between the severity of the stenosis, if present, in the aortic-iliac-femoral arteries and that in the coronary arteries (P less than 0.001). The subjects who did exhibit aortic-iliac-femoral arterial disease were significantly older and more frequently were cigarette smokers. We conclude that subjects with coronary arterial stenosis frequently are free of peripheral arterial disease.

Myocardial infarction and percent arteriographic stenosis of culprit lesion: report from the Program on the Surgical Control of the Hyperlipidemias (POSCH).

The objective of this study was to assess the percent stenosis of the culprit lesion responsible for subsequent myocardial infarction in the Program on the Surgical Control of the Hyperlipidemias (POSCH). It is unknown if the susceptible coronary artery culprit lesion responsible for an acute myocardial infarction is relatively large ( > or = 50% arteriographic stenosis) and hemodynamically significant ( > or = 70% stenosis), or small ( < 50%, stenosis) and asymptomatic. Certain necropsy and arteriography studies support the large progenitor lesion concept, and other arteriography studies support the small lesion hypothesis. We analyzed the coronary arteriogram immediately preceding a Q wave (transmural) myocardial infarction for the degree of stenosis of the suspected culprit lesion, which was selected by visual inspection of the coronary circulation supplying the electrocardiogram-defined area of myocardial infarction. There was no perceptible difference with respect to vessel segment distribution of culprit lesions or time to infarction between the 52 control-group patients and the 27 intervention-group patients. For the two groups combined (n=79), the predominantly involved segments were the middle right coronary artery and the proximal left anterior descending coronary artery. The time interval from the preceding coronary arteriogram closest to the index myocardial infarction ranged from 0 days to 10 years; however, 64.6% of the arteriograms were performed 2 years or less prior to the myocardial infarction. Only 5.1% of the patients in both groups combined had a culprit lesion stenosis < 50%, while 88.6% of the patients in both groups combined had a culprit lesion stenosis > or = 70%. The results strongly favor the large lesion hypothesis of causation for myocardial infarction. It is premature, however, to state that the relative size of the culprit lesion has been indisputably determined. The resolution of this problem has exceedingly important practical implications for the management of patients with known atherosclerotic coronary heart disease and for those asymptomatic individuals with silent atherosclerotic coronary heart disease.

Relation between Q-QS changes on the rest electrocardiogram and left ventricular function with healed myocardial infarction.

In the Program of Surgical Control of Hyperlipidemia, the relation of the Minnesota Q-QS codes for rest electrocardiograms to left ventricular (LV) function was studied in patients with healed myocardial infarction (MI). Of 838 subjects enrolled in the study, 477 (57%) had codable Q-QS patterns at the time of randomization. There was an extremely high correlation between the level of the Minnesota code and concurrent LV function, the latter being determined on left ventriculography by both ejection fraction and the number of segmental wall motion abnormalities. Subjects without a Q-QS code had less myocardial damage than did those with a code present in a single cardiac area. Extent of LV damage correlated with the level of significance of the Q-QS code, and when the code was present in only 1 cardiac location damage was greatest if the anteroseptal area was involved. Q-QS codes present in 2 rather than 1 cardiac area were associated with an even greater degree of LV damage. A previous study has shown a strong correlation between LV function and the Minnesota codes when the latter were recorded 0.5 to 5 years (mean 2.2) earlier at the time of the acute MI. The present data show that the relation between LV function and the Minnesota codes after an acute MI persists over time and is even stronger when both are determined in the healed state at a time remote from the acute event.

Comparison of exercise-positive with recovery-positive treadmill graded exercise tests.

A treadmill exercise test response may become positive because a diagnostic electrocardiographic ST-segment shift occurred during exercise, or, less often, because it occurred only during the recovery period after exercise had been completed. Factors that may be related to these 2 different responses in subjects enrolled in the Program of Surgical Control of Hyperlipidemia were investigated. No differences were found with regard to age, sex, level or location of Minnesota electrocardiographic Q-QS codes, number of narrowed coronary arteries, presence of collateral coronary artery circulation, ejection fraction, number of abnormally moving left ventricular wall segments, heart rate, systolic and diastolic blood pressure, double product, total exercise time, exercise-induced angina, or maximally achieved exercise heart rate or double product. Thus, the same significance should be attributed to a recovery-positive as to an exercise-positive treadmill test, and electrocardiographic, hemodynamic and angiocardiographic variables do not distinguish between subjects who exhibit these 2 different responses.

Correlation of electrocardiographic and pathologic findings in healed myocardial infarction.

A correlative study in 50 cases of healed myocardial infarction compared the 12 lead electrocardiogram with pathologic observations. The electrocardiogram was interpreted according to established Minnesota codes with some modifications. The following conclusions were reached: (1) The electrocardiogram underestimates the extent of myocardial infarction. (2) When a healed myocardial infarct at a specific location is recognized with electrocardiographic criteria, it is likely that there are unrecognized infarcts involving other areas of the left ventricle. (3) Infarctions involving the lateral and inferobasal areas are frequently unrecognized. (4) The electrocardiogram is more likely to miss myocardial infarcts in patients with multiple, than in those with single, electrocardiographically diagnosed infarcts. (5) Apical myocardial infarction does not appear to have specific electrocardiographic findings, other than those related to general infarct localization by electrocardiogram, particularly in patients with anteroseptal or anterolateral infarction. (6) Abnormal Q waves, generally thought to indicate transmural myocardial infarction, are frequently found in subendocardial infarction. (7) The simplified electrocardiographic classification of myocardial infarct site (anteroseptal, inferior, anterolateral) used in this study is preferable to more detailed classifications previously suggested by others.

Genetic factors in the electrocardiogram and heart rate of twins reared apart and together.

Important physiologic mechanisms have been thought not to exhibit large amounts of variability, due in part to the assumption that critical biologic functions will have evolved to an evolutionary optimum. The attainment of this optimum would necessarily eliminate individual differences in these variables. Using a sample of monozygotic and dizygotic twins reared apart since birth or early infancy, 12-lead electrocardiographic recordings and vectorcardiograms were obtained. Values of these variables for monozygotic and dizygotic twins reared together were obtained from other studies. Maximum likelihood tests of genetic and environmental components of variation for PR interval, QRS duration, QT interval and ventricular rate indicated a significant contribution of genetic effects (most heritabilities ranged from 30 to 60%), with a negligible contribution from common familial environmental effects.

Directional ST-segment deviation in graded exercise tests correlated with motion of the individual segments of the left ventricular wall.

An exercise test may be characterized as positive because of the production of either electrocardiographic ST-segment depression or elevation. The relationship of exercise-induced ST-segment deviation to the specific motion abnormalities of the individual segments of the left ventricular wall was investigated. The first 280 subjects to enter the Program of Surgical Control of Hyperlipidemia were studied by treadmill exercise testing and left ventriculography. The results showed that exercise-induced ST-segment elevation could occur without evidence in the resting subject of either dyskinesia or aneurysm of the left ventricle, that the area of left ventricular damage was much greater in subjects with exercise-induced ST-segment elevation than in those with ST-segment depression, and that wall motion abnormalities were concentrated in the inferoposterior area in the group with ST-segment elevation, but were generally scattered throughout the left ventricular wall in the group with ST-segment depression.

Effect of anti-rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5'-triphosphatase and superoxide dismutase activation, and ultrastructural changes.

OBJECT: The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti-rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5'-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. METHODS: Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2-7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 microg) intraperitoneal injection of anti-rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. CONCLUSIONS: The results showed that neutralizing IL-6 bioactivity with anti-rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

A Q fever case mimicking crimean-congo haemorrhagic fever.

Coxiella burnetii is the bacterium that causes Q fever. Human infection is mainly transmitted from cattle, goats and sheep. The disease is usually self-limited. Pneumonia and hepatitis are the most common clinical manifestations. In this study, we present a case of Q fever from the western part of Turkey mimicking Crimean-Congo haemorrhagic fever (CCHF) in terms of clinical and laboratory findings.