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Background: Left ventricular false tendons (LVFTs) are chord-like structures that traverse the LV cavity and are generally considered to be benign. However, they have been associated with arrhythmias, LV hypertrophy and LV dilation in some small studies. We hypothesize that LVFTs are associated with LV structural and functional changes assessed by echocardiography., Methods: We retrospectively evaluated echocardiographic and clinical parameters of 126 patients identified as having LVFTs within the past 2 years and compared them to 85 age-matched controls without LVFTs., Results: There were no significant differences in age (52 ± 18 versus 54 ± 18 years, P = 0.37), sex (55% versus 59% men, P = 0.49), race (36% versus 23% white, P = 0.07), systolic blood pressure (131 ± 22 versus 132 ± 23mmHg, P = 0.76) or body mass index (BMI, 31 ± 8 versus 29 ± 10kg/m 2 , P = 0.07) between controls and patients with LVFTs, respectively. Patients with LVFTs had more prevalent heart failure (43% versus 21%, P = 0.001). Patients with LVFTs had more LV dilation, were 2.5 times more likely to have moderate-to-severe mitral regurgitation, had more severe diastolic dysfunction and reduced LV systolic function (18% lower) compared with controls (all P < 0.05). After adjustment for covariates, basal and middle LVFT locations were associated with reduced LV systolic function (P < 0.01), and middle LVFTs were associated with LV dilation (P < 0.01)., Conclusions: Our findings suggest that LVFTs may not be benign variants, and basal and middle LVFTs may have more deleterious effects. Further prospective studies should be performed to determine their pathophysiological significance and whether they play a causal role in LV dysfunction., (Copyright © 2017 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

The availability of techniques such as surgical reperfusion, angioplasty, and thrombolysis for the treatment of acute myocardial infarction (AMI) has revived interest in seeking an early detectable biochemical marker diagnostic for AMI. Therefore, we investigated whether an unidentified oxidase that is released by activated neutrophils at the onset of AMI could be used as an early diagnostic assay. The conversion by plasma oxidase of 1 microM of adrenaline to 1 microM of adrenochrome represents the plasma oxidase activity (POA) of 1 U/L. Fifty patients suspected of having AMI, 40% of whose electrocardiograms were nondiagnostic for AMI, were admitted to the coronary care unit, and venous blood samples were obtained for determination of the POA and creatine phosphokinase-MB levels. Healthy volunteers (n = 12) served as control subjects, and 8 patients with pneumonia whose leukocyte counts were greater than 15,000 microL were included in the study. In those with AMI (n = 22), as determined by serial creatine phosphokinase-MB, the mean POA (+/- standard error of the mean) was 233 +/- 13 U/L, and in those with angina and no AMI (n = 28) was 127 +/- 5 U/L (P < 0.0001). In the control group, mean POA (+/- standard error of the mean) was 84 +/- 5 U/L (control versus angina; P < 0.01) and for those with infection was 214 +/- 10 U/L. At admission, the creatine phosphokinase-MB was diagnostic for only 12 of the 22 patients with AMI (sensitivity rate of 54%), whereas in 21 of those patients, the POA values were diagnostic for AMI (sensitivity rate of 95%).(ABSTRACT TRUNCATED AT 250 WORDS)

A clinical observation of chest pain associated with the onset of rate-related left bundle branch block has been described in patients with normal coronary arteriograms. The authors used standard cardiac rehabilitation techniques for exercise training in a 47-year-old woman with these manifestations. Serial treadmill tests revealed that during the course of 3 months of exercise training, the heart rate at onset of LBBB gradually rose from 133 to 175 beats per minute, and she no longer developed symptoms during her routine daily activities or exercises. Exercise training was a successful nonpharmacologic strategy that delayed the onset of rate-related LBBB and chest pain in this patient and avoided the need for beta blocker therapy.