BackgroundSurgical treatment of thoracic outlet syndrome (TOS) is necessary when non-surgical treatments fail. Complications of surgical procedures vary from short-term post-surgical pain to permanent disability. The outcome of TOS surgery is affected by the visibility during the operation. In this study, we have compared the complications arising during the supraclavicular and the transaxillary approaches to determine the appropriate approach for TOS surgery.MethodsIn this study, 448 patients with symptoms of TOS were assessed. The male-to-female ratio was approximately 1:4, and the mean age was 34.5 years. Overall, 102 operations were performed, including unilateral, bilateral, and reoperations, and the patients were retrospectively evaluated. Of the 102 patients, 63 underwent the supraclavicular approach, 32 underwent the transaxillary approach, and 7 underwent the transaxillary approach followed by the supraclavicular approach. Complications were evaluated over 24 months.ResultsThe prevalence of pneumothorax, hemothorax, and vessel injuries in the transaxillary and the supraclavicular approaches was equal. We found more permanent and transient brachial plexus injuries in the case of the transaxillary approach than in the case of the supraclavicular approach, but the difference was not statistically significant. Persistent pain and symptoms were significantly more common in patients who underwent the transaxillary approach (p<0.05).ConclusionThe supraclavicular approach seems to be the more effective technique of the two because it offers the surgeon better access to the brachial plexus and a direct view. This approach for a TOS operation offers a better surgical outcome and lower reoperation rates than the transaxillary method. Our results showed the supraclavicular approach to be the preferred method for TOS operations.

BackgroundHypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy, disarray, fibrosis, and increased risk for ventricular arrhythmias. Increased QT dispersion has been reported in patients with HCM, but the underlying mechanisms have not been completely elucidated. In this study, we examined the relationship between diffuse interstitial fibrosis, replacement fibrosis, QTc dispersion and ventricular arrhythmias in patients with HCM. We hypothesized that fibrosis would slow impulse propagation and increase dispersion of ventricular repolarization, resulting in increased QTc dispersion on surface electrocardiogram (ECG) and ventricular arrhythmias.MethodsECG and cardiac magnetic resonance (CMR) image analyses were performed retrospectively in 112 patients with a clinical diagnosis of HCM. Replacement fibrosis was assessed by measuring late gadolinium (Gd) enhancement (LGE), using a semi-automated threshold technique. Diffuse interstitial fibrosis was assessed by measuring T1 relaxation times after Gd administration, using the Look–Locker sequence. QTc dispersion was measured digitally in the septal/anterior (V1–V4), inferior (II, III, and aVF), and lateral (I, aVL, V5, and V6) lead groups on surface ECG.ResultsAll patients had evidence of asymmetric septal hypertrophy. LGE was evident in 70 (63%) patients; the median T1 relaxation time was 411±38 ms. An inverse correlation was observed between T1 relaxation time and QTc dispersion in leads V1–V4 (p<0.001). Patients with HCM who developed sustained ventricular tachycardia had slightly higher probability of increased QTc dispersion in leads V1–V4 (odds ratio, 1.011 [1.004–1.0178, p=0.003). We found no correlation between presence and percentage of LGE and QTc dispersion.ConclusionDiffuse interstitial fibrosis is associated with increased dispersion of ventricular repolarization in leads, reflecting electrical activity in the hypertrophied septum. Interstitial fibrosis combined with ion channel/gap junction remodeling in the septum could lead to inhomogeneity of ventricular refractoriness, resulting in increased QTc dispersion in leads V1–V4.

Anatomic characteristics specific to HCM hearts contribute to lower correlations between MBF/MFR values obtained by PMod and QPET, compared with non-HCM patients. These differences indicate that PMod and QPET cannot be used interchangeably for MBF/MFR analyses in HCM patients.

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