Prehospital pathways of occipital stroke patients with mainly visual symptoms.

OBJECTIVES: Occipital ischemic strokes typically cause homonymous visual field defects, for which means of rehabilitation are limited. Intravenous thrombolysis is increasingly and successfully used for their acute treatment. However, recognition of strokes presenting with mainly visual field defects is challenging for both patients and healthcare professionals. We studied prehospital pathways of occipital stroke patients with mainly visual symptoms to define obstacles in their early recognition. MATERIALS & METHODS: This observational, retrospective, registry-based study comprises occipital stroke patients with isolated visual symptoms treated at the neurological emergency department of Helsinki University Central Hospital in 2010-2015. We analyzed their prehospital pathways, including time from symptom onset to admission at the neurological emergency department (ODT), the number of points of care, the percentage of patients with ODT≤4.5 hours, and factors associated with delay. RESULTS: Among 245 patients, only 20.8% arrived within 4.5 hours and 6.5% received IV thrombolysis. Delayed arrival was most often due to patients' late contact to health care. Of the patients, 27.3% arrived through at least two points of care, and differential diagnostics to ophthalmologic disorders proved particularly challenging. ODT≤4.5 hours was associated with EMS utilization, direct arrival, and atrial fibrillation; a visit at an ophthalmologist and initial misdiagnosis were associated with ODT>4.5 hours. After multivariable analysis, only direct arrival predicted ODT≤4.5 hours. CONCLUSIONS: Occipital stroke patients with visual symptoms contact health care late, are inadequately recognized, and present with complex prehospital pathways. Consequently, they are often ineligible for IV thrombolysis. This presents a missed opportunity for preventing permanent visual field defects.

In-hospital cardiac complications after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Data on cardiac complications and their precipitants after intracerebral hemorrhage are scarce. We examined the frequency and risk factors for serious in-hospital cardiac events in a large cohort of consecutive intracerebral hemorrhage patients. METHODS: A retrospective chart review of 1013 consecutive patients with nontraumatic intracerebral hemorrhage treated at the Helsinki University Central Hospital (2005-2010). We excluded patients with intraparenchymal hematoma related to sub-arachnoid hemorrhage or intracerebral hemorrhage because of fibrinolytic therapies for acute ischemic stroke or myocardial infarction. Serious in-hospital cardiac event was defined as any of in-hospital poststroke acute myocardial infarction, ventricular fibrillation or tachycardia, moderate to serious acute heart failure, or cardiac death. RESULTS: Among the 948 patients included, ≥1 serious in-hospital cardiac event occurred in 39 (4·1%) patients after a median delay of two-days from stroke onset (acute myocardial infarction in three patients, ventricular fibrillation or tachycardia in three patients, acute heart failure in 36 patients, and cardiac death in three patients). Hospital stay was longer in patients with serious in-hospital cardiac event than in those without (median 12, interquartile range 7-19 vs. 8, 3-14; P = 0·001), with no difference in in-hospital mortality (23·1% vs. 24·3%; P = 0·86). In multivariable logistic regression analysis adjusted for age, gender, and diabetes, atrial fibrillation during hospitalization (odds ratio 6·68 for new-onset atrial fibrillation, 95% confidence interval 2·11-21·18; 4·46 for old atrial fibrillation, 2·08-9·56), and history of myocardial infarction (3·20, 1·18-8·66) were independently associated with serious in-hospital cardiac events. CONCLUSIONS: After intracerebral hemorrhage, 4% of patients suffer an acute serious cardiac complication. Those with history of myocardial infarction or in-hospital atrial fibrillation are at greater risk for such events.

The cardiac troponin I gene is not associated with hypertrophic cardiomyopathy in patients from eastern Finland.

Defects in seven genes encoding sarcomere proteins have been shown to cause hypertrophic cardiomyopathy. To date, only one study reporting defects in the cardiac troponin I gene associated with hypertrophic cardiomyopathy has been published, and the proportion of hypertrophic cardiomyopathy cases caused by defects in this gene is unknown. Therefore, the authors screened 37 unrelated Finnish patients with hypertrophic cardiomyopathy for variants in the cardiac troponin I gene. Exons 1-8 of the troponin I gene were screened with the polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) method. Five different variants (four intron variants and one silent exon variant) were found. Most variants were also present in control samples and none of the variants co-segregated with the disease in families. The results of the present study indicate that defects in the cardiac troponin I gene do not cause hypertrophic cardiomyopathy in patients from Eastern Finland.

The cardiac beta-myosin heavy chain gene is not the predominant gene for hypertrophic cardiomyopathy in the Finnish population.

OBJECTIVES: The aim of the study was to screen 36 unrelated patients with hypertrophic cardiomyopathy (HCM; 16 familial and 20 sporadic cases) from a genetically homogeneous area in eastern Finland for variants in the cardiac beta-myosin heavy chain (beta-MHC) and alpha-tropomyosin (alpha-TM) genes. BACKGROUND: Mutations in the beta-MHC and alpha-TM genes have been reported to be responsible for 30% to 40% and less than 5% of familial HCM cases, respectively. However, most genetic studies have included patients from tertiary care centers and are subject to referral bias. METHODS: Exons 3-26 and 40 of the beta-MHC gene and the nine exons of the alpha-TM gene were screened with the PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) method. Linkage analyses between familial HCM locus and two intragenic polymorphic markers (MYO I and MYO II) of the beta-MHC gene were performed in 16 familial HCM kindreds. RESULTS: A previously reported Arg719Trp (arginine converted to tryptophan in codon 719) mutation of the beta-MHC gene was found in one proband and two relatives. In addition, a novel Asn696Ser (asparagine converted to serine in codon 696) substitution was found in one HCM patient. No linkage between familial HCM and the beta-MHC gene was observed in 16 familial kindreds. A previously reported Aspl75Asn (aspartic acid converted to asparagine in codon 175) mutation of the alpha-TM gene was found in four probands and 16 relatives. Mutations in the beta-MHC and alpha-TM genes accounted for 6% and 25% familial HCM cases and 3% and 11% of all cases, respectively. CONCLUSIONS: Our results indicate that the beta-MHC gene is not the predominant gene for HCM in the Finnish population, whereas HCM caused by the Aspl75Asn mutation of the a-TM gene is more common than previously reported.