Running on the Edge: Rupture of the Tibialis Anterior Muscle During an Ultramarathon.

A 47-year-old male ultramarathon runner presented with persistent discomfort in the anterior region of the left leg. The patient reported a snapping sensation in his left leg four weeks earlier while running an ultramarathon, followed by ecchymosis and functional impairment the next day. Physical examination revealed a palpable area of fibrosis in his anterior left leg. Ultrasound of the left leg identified a partially organized rupture of the distal third of the tibialis anterior muscle. The rupture had an extension of 36 x 10 x 27mm with associated muscle edema. The patient was treated non-surgically with a customized rehabilitation program and later returned to ultramarathon running. This case illustrates the importance of proper differential diagnosis and individualized rehabilitation programs to achieve optimum clinical and functional results.

Prognostic implications of fibrosis in low risk aortic stenosis patients.

INTRODUCTION AND OBJECTIVES: Among patients with aortic stenosis (AS), interstitial fibrosis has been associated with progression to heart failure and is a marker of poorer prognosis. We aimed to assess the impact of myocardial fibrosis on clinical events after aortic valve replacement (AVR) in low risk, severe AS. METHODS: We prospectively followed 56 severe AS patients with ejection fraction >40%, who underwent AVR with simultaneous myocardial biopsies and collagen volume fraction (CVF) determination. Baseline and follow-up echocardiographic parameters were assessed. Outcomes were all-cause death and the combined endpoint of all-cause death or non-fatal cardiovascular hospitalization. RESULTS: Patients were predominantly women (67.9%) and mean age was 66±12 years. At follow-up, there was a significant decrease in transaortic gradients and wall stress, as well as regression in indexed LV mass. Patients who suffered a fatal event or the combined endpoint had a higher degree of fibrosis (27.1±20.7% vs. 15.4±11.8%, p=0.035; 24.0±18.2% vs. 15.3±12.0%, p=0.038, respectively). Patients with CVF≥15.4% had higher rates of all-cause death (37.5% vs. 97.0%, p=0.001) and lower survival free of the combined endpoint of all-cause death or non-fatal cardiovascular hospitalization (0% vs. 91.2%, p<0.001). CVF was the only independent predictor of all-cause death (hazard ratio (HR) 1.88; 95% confidence interval (CI): 1.08-3.29 for each 10% increase; p=0.026) and all-cause death or cardiovascular hospitalization (HR 1.73; 95% CI: 1.03-2.911 for each 10% increase; p=0.038). CONCLUSIONS: In low risk AS patients, higher levels of fibrosis are independent predictors of all-cause death and the composite of all-cause death or non-fatal cardiovascular hospitalization. Further advances in anti-fibrotic therapies in AS are needed.

Severe Pneumonia Caused by SARS-CoV-2: A Novel Cause of Platypnoea-Orthodeoxia Syndrome.

Platypnoea-orthodeoxia syndrome (POS) is a condition characterized by dyspnoea and hypoxaemia while sitting or standing, which improves during decubitus. It is usually caused by intracardiac right-to-left shunting through a patent foramen ovale but may also occur due to pulmonary ventilation-perfusion mismatch of other aetiologies. A new cause of POS was recently described: SARS-CoV-2 pneumonia. We report the case of a 62-year-old man admitted for SARS-CoV-2 pneumonia with respiratory failure. Chest computed tomography angiography showed pulmonary thromboembolism and parenchymal lung changes compatible with COVID-19. He had worsening dyspnoea in a sitting position, relieved by assuming the dorsal position. He was diagnosed with POS after other causes were excluded. POS is an underdiagnosed complication of COVID-19 and is manageable with respiratory rehabilitation. LEARNING POINTS: Platypnoea-orthodeoxia syndrome is an under-recognized condition presenting as a complication of a structural shunt.We describe SARS-CoV-2 pneumonia as a novel cause for this syndrome.It is a reversible syndrome provided there is early diagnosis and initiation of pulmonary rehabilitation.

MicroRNAs and ventricular remodeling in aortic stenosis.

INTRODUCTION AND OBJECTIVES: Several mechanisms contribute to myocardial hypertrophy and fibrosis in aortic stenosis (AS). MicroRNAs are post-transcriptional modulators of such processes. We hypothesized that their expression in myocardial biopsies from patients with AS could be linked with the degree of left ventricular (LV) hypertrophy and remodeling and to plasma levels of important biomarkers of extracellular matrix turnover. METHODS: We performed myocardial biopsies in eleven patients with isolated severe AS undergoing aortic valve replacement. Echocardiographic exams and biomarker quantification were also performed. Five explanted hearts were used as controls for microRNA expression. RESULTS: Overexpression of microRNA-101-3p was found in AS, which correlated with higher levels of preoperative valvuloarterial impedance, angiotensin II receptor and angiotensin-converting enzyme, and LV mass regression after surgery. Although not differently expressed in AS compared to controls, both upregulation of miR-4268 and downregulation of microRNA-125-5p were associated with higher LV mass. MicroRNA-125b-5p correlated negatively with LV mass and with relative wall thickness at six-month follow-up. MicroRNA-4268 correlated positively with LV mass regression and was associated with higher plasma angiotensin II receptor levels. CONCLUSIONS: MicroRNA-101-3p and microRNA-4268 have potential new roles in the modulation of the hypertrophic response to AS via the renin-angiotensin-aldosterone system and as predictors of reverse remodeling after aortic valve replacement. Our results open new avenues in the understanding of myocardial response to pressure overload and of reverse remodeling after unloading. They also support the possibility of medical therapy to modulate the renin-angiotensin-aldosterone system in hypertrophic hearts.