Scalp Reconstruction Using the Latissimus Dorsi Free Flap: A 12-Year Experience.

BACKGROUND: Complex scalp defects are regularly reconstructed using microvascular tissue transfer. The latissimus dorsi free flap is one of the workhorse flaps used in scalp reconstruction. These cases necessitate, particularly in the elderly, a close cooperation between plastic surgeons and neurosurgeons. The purpose of this study was to evaluate the suitability of the latissimus dorsi free flap for complex scalp reconstructions and to analyze potential risk factors. METHODS: A retrospective study identified 43 patients undergoing complex scalp reconstruction using a latissimus dorsi free flap at our department between 2010 and 2022. RESULTS: The mean patient age was 61 ± 18 years. Defects were mostly caused by oncologic tumor resections (n = 23; 55%), exposure to a cranioplasty (n = 10; 23%) or infection (n = 4; 9%). The most frequent recipient vessels were the superficial temporal artery (n = 28; 65%), external carotid artery (n = 12; 28%) and the venae comitantes (n = 28; 65%), external jugular vein (n = 6; 14%). The reconstructive success rate was 97.7%. There was one total flap loss (2%). Partial flap loss occurred in five cases (12%). Follow-up was 8 ± 12 months. Major complications were seen in 13 cases, resulting in a revision rate of 26%. Multivariate logistic regression identified active tobacco use as the only risk factor for major complications (odds ratio 8.9; p = 0.04). CONCLUSION: Reconstruction of complex scalp defects using the latissimus dorsi free flap yielded high success rates. Among the potential risk factors, active tobacco use seems to affect the outcome of complex scalp reconstructions.

Validation of the German version of the subarachnoid haemorrhage outcome tool (SAHOT).

Objective: The subarachnoid haemorrhage (SAH) outcome tool (SAHOT) is the first SAH-specific patient reported outcome measure, and was developed in the UK. We aimed to validate the SAHOT outside the UK, and therefore endeavored to adapt the SAHOT into German and to test its psychometric properties. Methods: We adapted and pilot tested the German version. We applied the SAHOT, Quality of Life after Brain Injury, Hospital Anxiety and Depression Scale, and EuroQol questionnaires in a cohort of 89 patients with spontaneous SAH after discharge. We assessed internal consistency by Cronbach's α, test-retest reliability by intraclass correlation, and validity by Pearson correlations with established measures. Sensitivity to change was evaluated following neurorehabilitation by effect sizes. Results: The translation of SAHOT resulted in a German version that is semantically and conceptually equivalent to the English version. Internal consistency was good regarding the physical domain (α = 0.83) and excellent for the other domains (α = 0.92-0.93). Test-retest reliability indicated a high level of stability with an intraclass correlation of 0.85 (95% CI: 0.83-0.86). All domains correlated moderately or strongly with established measures (r = 0.41-0.74; p < 0.01). SAHOT total scores showed moderate sensitivity to change (Cohen's d = -0.68), while mRS and GOSE showed no significant sensitivity to change. Conclusion: The SAHOT can be adapted to other health care systems and societies than the UK. The German version of the SAHOT is a reliable and valid instrument, and can be used in future clinical studies and individual assessment after spontaneous SAH.

Atrial myofibroblast activation and connective tissue formation in a porcine model of atrial fibrillation and reduced left ventricular function.

AIMS: Atrial fibrillation (AF) is associated with fibrosis that slows electrical conduction and causes perpetuation of the arrhythmia. The molecular characterization of AF pathophysiology may provide novel therapeutic options. This study was designed to elucidate profibrotic signaling and myofibroblast activation in a porcine model of atrial tachypacing-induced AF and reduced left ventricular function. MATERIALS AND METHODS: Ten domestic pigs were randomized to sinus rhythm (SR) or AF groups. Prior to AF induction and on day 14 the animals underwent echocardiographic examinations. Profibrotic pathways were analyzed in right atrial tissue obtained from AF animals compared to SR controls using histology, immunofluorescence microscopy, Western blot, and real-time PCR. KEY FINDINGS: AF was associated with atrial dilation, increased atrial fibrosis, and enhanced expression of collagens I and V in right atrial tissue after 14days follow-up. The fraction of α-smooth muscle actin (SMA)-producing activated myofibroblasts was elevated in AF, whereas the abundance of vimentin-expressing inactive fibroblasts was not affected. Profibrotic signaling involved upregulation of TGF-ß1, Smad2/3, and CTGF. SIGNIFICANCE: The transformation of atrial fibroblasts into myofibroblasts through activation of TGF-ß1 and CTGF emerged as potential cellular trigger of fibrogenesis. Prevention of fibroblast-to-myofibroblast switching may serve as target for remodeling-based antiarrhythmic AF therapy.

TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control.

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Concomitant heart failure (HF) poses a particular therapeutic challenge and is associated with prolonged atrial electrical refractoriness compared with non-failing hearts. We hypothesized that downregulation of atrial repolarizing TREK-1 (K2P2.1) K+ channels contributes to electrical remodeling during AF with HF, and that TREK-1 gene transfer would provide rhythm control via normalization of atrial effective refractory periods in this AF subset. In patients with chronic AF and HF, atrial TREK-1 mRNA levels were reduced by 82% (left atrium) and 81% (right atrium) compared with sinus rhythm (SR) subjects. Human findings were recapitulated in a porcine model of atrial tachypacing-induced AF and reduced left ventricular function. TREK-1 mRNA (-66%) and protein (-61%) was suppressed in AF animals at 14-day follow-up compared with SR controls. Downregulation of repolarizing TREK-1 channels was associated with prolongation of atrial effective refractory periods versus baseline conditions, consistent with prior observations in humans with HF. In a preclinical therapeutic approach, pigs were randomized to either atrial Ad-TREK-1 gene therapy or sham treatment. Gene transfer effectively increased TREK-1 protein levels and attenuated atrial effective refractory period prolongation in the porcine AF model. Ad-TREK-1 increased the SR prevalence to 62% during follow-up in AF animals, compared to 35% in the untreated AF group. In conclusion, TREK-1 downregulation and rhythm control by Ad-TREK-1 transfer suggest mechanistic and potential therapeutic significance of TREK-1 channels in a subgroup of AF patients with HF and prolonged atrial effective refractory periods. Functional correction of ionic remodeling through TREK-1 gene therapy represents a novel paradigm to optimize and specify AF management.

Atrial fibrillation complicated by heart failure induces distinct remodeling of calcium cycling proteins.

Atrial fibrillation (AF) and heart failure (HF) are two of the most common cardiovascular diseases. They often coexist and account for significant morbidity and mortality. Alterations in cellular Ca2+ homeostasis play a critical role in AF initiation and maintenance. This study was designed to specifically elucidate AF-associated remodeling of atrial Ca2+ cycling in the presence of mild HF. AF was induced in domestic pigs by atrial burst pacing. The animals underwent electrophysiologic and echocardiographic examinations. Ca2+ handling proteins were analyzed in right atrial tissue obtained from pigs with AF (day 7; n = 5) and compared to sinus rhythm (SR) controls (n = 5). During AF, animals exhibited reduction of left ventricular ejection fraction (from 73% to 58%) and prolonged atrial refractory periods. AF and HF were associated with suppression of protein kinase A (PKA)RII (-62%) and Ca2+-calmodulin-dependent kinase II (CaMKII) δ by 37%, without changes in CaMKIIδ autophosphorylation. We further detected downregulation of L-type calcium channel (LTCC) subunit α2 (-75%), sarcoplasmic reticulum Ca2+-ATPase (Serca) 2a (-29%), phosphorylated phospholamban (Ser16, -92%; Thr17, -70%), and phospho-ryanodine receptor 2 (RyR2) (Ser2808, -62%). Na+-Ca2+ exchanger (NCX) levels were upregulated (+473%), whereas expression of Ser2814-phosphorylated RyR2 and LTCCα1c subunits was not significantly altered. In conclusion, AF produced distinct arrhythmogenic remodeling of Ca2+ handling in the presence of tachycardia-induced mild HF that is different from AF without structural alterations. The changes may provide a starting point for personalized approaches to AF treatment.