Long-term Posttraumatic Survival of Spinal Fracture Patients in Northern Finland.

STUDY DESIGN: A retrospective epidemiological study. OBJECTIVE: To reveal the long-term survival and causes of death after traumatic spinal fracture (TSF) and to determine the possible factors predicting death. SUMMARY OF BACKGROUND DATA: Increased mortality following osteoporotic spinal fracture has been represented in several studies. Earlier studies concerning mortality after TSF have focused on specific types of fractures, or else only the mortality of the acute phases has been documented. In-hospital mortality has varied between 0.1% and 4.1%. METHODS: The study sample of 947 patients including all patients with TSF admitted to Oulu University Hospital, Finland, between January 1, 2007 and December 31, 2011. TSFs were identified using International Classification of Diseases 10th revision or Nordic Classification of Surgical Procedures codes and all patient records were manually reviewed. Times and causes of death, obtained from Statistics Finland's Archive of Death Certificates, were available until the end 2016 and 2015, respectively. RESULTS: At the end of the follow-up 227 (24.0%) had died. Mortality was 6.8% after the first year and 19.1% after 5 years. Mortality was increased in all age groups compared with the general population, 1-year standardized mortality ratios ranging from 3.1 in over 65-year-olds to 19.8 in under 30-year-olds. In age groups of 50 to 64 years and over 65 years, the most important risk factors for death were males with hazard ratios of 3.0 and 1.6, respectively, and low fall as trauma mechanism with hazard ratios of 9.4 and 10.2, respectively. CONCLUSION: Traumatic spinal fractures are associated with increased mortality compared with the general population, high mortality focusing especially on older people and men. The increase seems to be comparable to the increase following hip fracture. Patients who sustain spinal fracture due to falling need special attention in care, due to the observation that low fall as trauma mechanism increased the risk of death significantly. LEVEL OF EVIDENCE: 3.

Traumatic Spinal Injuries in Northern Finland.

STUDY DESIGN: A retrospective epidemiological study. OBJECTIVE: To reveal incidence and epidemiological features of traumatic spinal injuries (TSI) in Northern Finland. SUMMARY OF BACKGROUND DATA: In Finland the annual incidence of traumatic spine fractures requiring inpatient care has been found to be 27/100,000, while international incidences have varied across the range of 16-64/100,000. More specific epidemiological data from Finland is not available. Internationally, the most common mechanisms of injury are road traffic as well as low and high falls. Associated injuries occur in 30% to 55% of cases. METHODS: The study sample included patients with traumatic spinal injury admitted to Oulu University Hospital (OYS) with injury between the January 1, 2007 and December 31, 2011. Patient information was collected from the hospital care register, including all inpatient and outpatient visits and surgical procedures. Traumatic spinal column and spinal cord injuries were identified using International Classification of Diseases 10th revision or Nordic Classification of Surgical Procedures codes and all patient records were manually reviewed. RESULTS: Nine hundred seventy-one patients met the criteria for TSI. The mean annual incidence of hospitalized traumatic spinal injuries was 26/100,000 in the whole of Northern Finland and 35/100,000 in the OYS main responsibility area. The most frequent etiology of TSI was low falls, which accounted for 35.8% of the injuries, followed by road traffic and high falls. Lumbar spine was the most common site of the fracture. Spinal surgery was performed in 376 (38.7%) cases. Three hundred eight patients (31.7%) suffered from associated injuries, 101 (10.4%) had a spinal cord injury, and 71 (7.3%) a brain injury. CONCLUSION: Low falls in elderly and road traffic injuries in younger age groups were the most common etiology of traumatic spinal injuries in Northern Finland and should be given more attention in primary prevention. LEVEL OF EVIDENCE: 3.

Mitochondrial DNA Depletion and Deletions in Paediatric Patients with Neuromuscular Diseases: Novel Phenotypes.

OBJECTIVE: To study the clinical manifestations and occurrence of mtDNA depletion and deletions in paediatric patients with neuromuscular diseases and to identify novel clinical phenotypes associated with mtDNA depletion or deletions. METHODS: Muscle DNA samples from patients presenting with undefined encephalomyopathies or myopathies were analysed for mtDNA content by quantitative real-time PCR and for deletions by long-range PCR. Direct sequencing of mtDNA maintenance genes and whole-exome sequencing were used to study the genetic aetiologies of the diseases. Clinical and laboratory findings were collected. RESULTS: Muscle samples were obtained from 104 paediatric patients with neuromuscular diseases. mtDNA depletion was found in three patients with severe early-onset encephalomyopathy or myopathy. Two of these patients presented with novel types of mitochondrial DNA depletion syndromes associated with increased serum creatine kinase (CK) and multiorgan disease without mutations in any of the known mtDNA maintenance genes; one patient had pathologic endoplasmic reticulum (ER) membranes in muscle. The third patient with mtDNA depletion was diagnosed with merosine-deficient muscular dystrophy caused by a homozygous mutation in the LAMA2 gene. Two patients with an early-onset Kearns-Sayre/Pearson-like phenotype harboured a large-scale mtDNA deletion, minor multiple deletions and high mtDNA content. CONCLUSIONS: Novel encephalomyopathic mtDNA depletion syndrome with structural alterations in muscle ER was identified. mtDNA depletion may also refer to secondary mitochondrial changes related to muscular dystrophy. We suggest that a large-scale mtDNA deletion, minor multiple deletions and high mtDNA content associated with Kearns-Sayre/Pearson syndromes may be secondary changes caused by mutations in an unknown nuclear gene.

Endothelin-1 contributes to the Frank-Starling response in hypertrophic rat hearts.

Endothelin-1 is involved in mechanical load-induced cardiac growth processes; it also has effects on contractility. The interaction of endothelin-1 and the Frank-Starling response is unknown. The present study aimed to characterize the role of endothelin-1 in the regulation of the Frank-Starling response, one of the major mechanisms regulating cardiac contractile force, in both normal and hypertrophied hearts. Nontransgenic rat hearts and hypertrophic hearts of hypertensive double transgenic rats harboring human angiotensinogen and renin genes were studied in a Langendorff isolated heart setup with a liquid-filled balloon inside the left ventricle used to measure contractile parameters. The rats were studied at compensated phase, before showing any signs of heart failure. Compensated hypertrophy in double transgenic rat hearts resulted in improved contractility at a given level of preload when compared with nontransgenic rat hearts. Hearts of both rat lines showed preserved Frank-Starling responses, that is, increased contractile function in response to increased end-diastolic pressure. The mixed endothelin A/B receptor antagonist bosentan attenuated the Frank-Starling response by 53% (P<0.01) in the double transgenic hearts but not in nontransgenic hearts. The diastolic parameters remained unaffected. The left ventricles of the double transgenic rat hearts showed an 82% higher level of endothelin type A receptor mRNA and a 25% higher level of immunoreactive endothelin-1 compared with nontransgenic rat hearts. The type 1 angiotensin II receptor antagonist CV-11974 had no significant effect on contractile function in response to load in either strain. These results show that endogenous endothelin-1 contributes to the Frank-Starling response in hypertrophied rat hearts by affecting systolic performance.