Obesity paradox in stroke – Myth or reality? A systematic review

<div><p>Background and purpose</p><p>Both stroke and obesity show an increasing incidence worldwide. While obesity is an established risk factor for stroke, its influence on outcome in ischemic stroke is less clear. Many studies suggest a better prognosis in obese patients after stroke (“obesity paradox”). This review aims at assessing the clinical outcomes of obese patients after stroke by performing a systematic literature search.</p><p>Methods</p><p>The reviewers searched MEDLINE from inception to December 2015. Studies were eligible if they included outcome comparisons in stroke patients with allocation to body weight.</p><p>Results</p><p>Twenty-five studies (299’750 patients) were included and none was randomised. Ten of 12 studies (162’921 patients) reported significantly less mortality rates in stroke patients with higher BMI values. Seven of 9 studies (92’718 patients) ascertained a favorable effect of excess body weight on non-fatal outcomes (good clinical outcome, recurrence of vascular events). Six studies (85’042 patients) indicated contradictory results after intravenous thrombolysis (IVT), however. Several methodological limitations were observed in major part of studies (observational study design, inaccuracy of BMI in reflecting obesity, lacking body weight measurement, selection bias, survival bias).</p><p>Conclusion</p><p>Most observational data indicate a survival benefit of obese patients after stroke, but a number of methodological concerns exist. No obesity paradox was observed in patients after IVT. There is a need for well-designed randomized controlled trials assessing the effects of weight reduction on stroke risk in obese patients.</p></div

Are 12-lead ECG findings associated with the risk of cardiovascular events after ischemic stroke in young adults?

<p><b>Introduction:</b> Ischemic stroke (IS) in a young patient is a disaster and recurrent cardiovascular events could add further impairment. Identifying patients with high risk of such events is therefore important. The prognostic relevance of ECG for this population is unknown.</p> <p><b>Materials and methods:</b> A total of 690 IS patients aged 15–49 years were included. A 12-lead ECG was obtained 1–14 d after the onset of stroke. We adjusted for demographic factors, comorbidities, and stroke characteristics, Cox regression models were used to identify independent ECG parameters associated with long-term risks of (1) any cardiovascular event, (2) cardiac events, and (3) recurrent stroke.</p> <p><b>Results:</b> Median follow-up time was 8.8 years. About 26.4% of patients experienced a cardiovascular event, 14.5% had cardiac events, and 14.6% recurrent strokes. ECG parameters associated with recurrent cardiovascular events were bundle branch blocks, P-terminal force, left ventricular hypertrophy, and a broader QRS complex. Furthermore, more leftward P-wave axis, prolonged QTc, and P-wave duration >120 ms were associated with increased risks of cardiac events. No ECG parameters were independently associated with recurrent stroke.</p> <p><b>Conclusion:</b> A 12-lead ECG can be used for risk prediction of cardiovascular events but not for recurrent stroke in young IS patients.KEY MESSAGES</p><p>ECG is an easy, inexpensive, and useful tool for identifying young ischemic stroke patients with a high risk for recurrent cardiovascular events and it has a statistically significant association with these events even after adjusting for confounding factors.</p><p>Bundle branch blocks, P-terminal force, broader QRS complex, LVH according to Cornell voltage duration criteria, more leftward P-wave axis, prolonged QTc, and P-wave duration >120 ms are predictors for future cardiovascular or cardiac events in these patients.</p><p>No ECG parameters were independently associated with recurrent stroke.</p><p></p> <p>ECG is an easy, inexpensive, and useful tool for identifying young ischemic stroke patients with a high risk for recurrent cardiovascular events and it has a statistically significant association with these events even after adjusting for confounding factors.</p> <p>Bundle branch blocks, P-terminal force, broader QRS complex, LVH according to Cornell voltage duration criteria, more leftward P-wave axis, prolonged QTc, and P-wave duration >120 ms are predictors for future cardiovascular or cardiac events in these patients.</p> <p>No ECG parameters were independently associated with recurrent stroke.</p

Source strength estimates (nAm) of ∼10-Hz activity over the temporo-parietal region in all patients (mean ± SEM), and low-frequency (∼1-Hz) oscillations in the patients, in whom low-frequency oscillations were detected (mean ± SEM).

<p>AH, affected hemisphere. UH, unaffected hemisphere. T₀, 1–7 days; T₁, 1 month, and T₂, 3 months after stroke. Ctrl., control subjects (hemispheres pooled).</p

Clinical details of the patients.

<p>AH, affected hemisphere. C, cortical. CS, cortico-subcortical. S, subcortical. Size, lesion volume in cm³. St, Peg, time (s). NIHSS; National Institutes of Health Stroke Scale (0–42 points). mRS, modified Rankin Scale (0–5 points). T₀, 1–7 days; T₂, 3 months after stroke.</p

Spectrum and source localization of abnormal low-frequency magnetic activity (ALFMA).

<p>A) Amplitude spectra (eyes closed) of spontaneous 0–5-Hz brain oscillations in one patient and one control subject. Two channels from the amplitude spectra of spontaneous 0–5-Hz brain oscillations in one patient at T₀, T₁, and T₂ and in one control subject. AH, channel from the perilesional area in the affected hemisphere. UH, channel from the corresponding region in the unaffected hemisphere. T₀, 1 week; T₁, 1month; T₂, 3 months after stroke. B) Source localization of ALFMA in one patient <i>above</i> Source localization of ALFMA (arbitrary scale) projected on the surface of the standard brain volume (same patient as in A). <i>below</i> Source localizations of ALFMA projected on the MRI of the patient. Lesion localization is shown on the left.</p

MRI based evaluation of the effect of oncolytic adenovirus Ad5-D24-RGD in metastatic colorectal cancer mouse model.

<p>1x10e6 HT29 cells were injected into the spleen of 125-day-old SCID mice. Intratumoral injection of the virus (OV) at a dose of 2x10e7 viral particles was given 21 days later (arrow). Intrasplenic tumor growth (A), number of metastatic lesions in the liver (B) and a total volume of liver metastasis (C) were assessed weekly with MRI. Data is presented as mean ± SD. *, p<0.05, **, p<0.01.</p

Developmental stage of the spleens of adult SCID and NMRI nude mice.

<p>125 to 135 days old SCID and NMRI nude mice from different providers were imaged with MRI to evaluate the developmental stage of the spleens (arrows). For SCID mice, animals purchased from Charles River (A) and Harlan (B) showed poorly developed, diffuse, and small spleens while animals from Taconic (C) had solid, compact, and relatively large spleens. NMRI nude mice from Charles River (D) and Scanbur (E) showed fully developed spleens with a similar appearance.</p

Morphology of the spleens of 30- and 125-day-old SCID and NMRI nude mice.

<p>SCID, severe combined immunodeficiency; NA, not applicable.</p

Frequencies (Hz) and amplitudes of spectral peaks in the patients (fT/cm√Hz) over the temporo-parietal (eyes open) and occipital (eyes closed) areas.

<p>AH, affected hemisphere. UH, unaffected hemisphere. f, frequency (Hz). A, amplitude (fT/cm√Hz) T₀, 1–7 days; T₁, 1 month, and T₂, 3 months after stroke. Ctrl., control subjects (right and left hemispheres pooled).</p

Amplitude spectra of one patient (gradiometers; eyes open).

<p>Three channels from both hemispheres, showing peaks of rolandic ∼10-Hz, rolandic beta, and occipital alpha activity. Rolandic ∼10-Hz oscillations are clearly increased in the affected hemisphere (AH). UH; unaffected hemisphere. T₀, 1 week; T₁, 1month; T₂, 3 months after stroke.</p