Autonomic dysfunction as a cause of cardiovascular disease

 

This free full text review focuses on neurodegenerative synucleinopathies and briefly, in addition, touches on other disorders such as POTS, vasovagal syncope and inappropriate sinus tachycardia.

Synucleinopathies result from misfolded protein aggregates of α-synuclein. The normal function of α-synuclein in the nervous system is not well understood.

The synucleinopathies are parkinson disease, lewy body dementia, pure autonomic failure and multiple system atrophy. Any of these disorders can be accompanied by autonomic dysfunction.

Orthostatic hypotension, supine hypertension, or both may occur. All of the long-term consequences of hypertension may be associated with the supine hypertension seen in autonomic dysfunction. Use of a short acting antihypertensive administered at night is a suggested treatment strategy.

Delirium in hospitalized patients predicts readmission and other forms of increased post hospital utilization

Report here.

This is not surprising, since delirium in the hospital is often a sign of frailty.

Syncope guidelines

Unbelievably long for what should be a simple topic, but everything you’re likely to want or need to know is here.

Strength training improved cognition in older patients

---in this study.

What explains strokes in young people (ages 18-55)?

Traditional, modifiable risk factors in almost 80% in this study.

Troponin elevation in stroke may point to a cardioembolic etiology

From a recent paper:

Abstract

Background Our aim was to determine whether patients with embolic strokes of undetermined source (ESUS) have higher rates of elevated troponin than patients with noncardioembolic strokes.

Methods and Results CAESAR (The Cornell Acute Stroke Academic Registry) prospectively enrolled all adults with acute stroke from 2011 to 2014. Two neurologists used standard definitions to retrospectively ascertain the etiology of stroke, with a third resolving disagreements. In this analysis we included patients with ESUS and, as controls, patients with small‐ and large‐artery strokes; only patients with a troponin measured within 24 hours of stroke onset were included. A troponin elevation was defined as a value exceeding our laboratory's upper limit (0.04 ng/mL) without a clinically recognized acute ST‐segment elevation myocardial infarction. Multiple logistic regression was used to evaluate the association between troponin elevation and ESUS after adjustment for demographics, stroke severity, insular infarction, and vascular risk factors. In a sensitivity analysis we excluded patients diagnosed with atrial fibrillation after discharge. Among 512 patients, 243 (47.5%) had ESUS, and 269 (52.5%) had small‐ or large‐artery stroke. In multivariable analysis an elevated troponin was independently associated with ESUS (odds ratio 3.3; 95% confidence interval 1.2, 8.8). This result was unchanged after excluding patients diagnosed with atrial fibrillation after discharge (odds ratio 3.4; 95% confidence interval 1.3, 9.1), and the association remained significant when troponin was considered a continuous variable (odds ratio for log[troponin], 1.4; 95% confidence interval 1.1, 1.7).

Conclusions Elevations in cardiac troponin are more common in patients with ESUS than in those with noncardioembolic strokes.

Unfortunately the test characteristics for determining cardioembolic stroke are poor. Most patients with cardioembolic stroke do not have elevated troponins and some with other types of stroke have elevations.

Targeted temperature management post arrest: how long?

Findings from a recent trial:

Question Does targeted temperature management at 33°C for 48 hours result in better neurologic outcome compared with standard 24-hour targeted temperature management in unconscious patients with out-of-hospital cardiac arrest?

Findings In this randomized clinical trial enrolling 355 adults with out-of-hospital cardiac arrest, there was no significant difference in favorable neurologic outcome at 6 months for those treated for 48 hours (69%) vs 24 hours (64%) (difference, 5%).

Meaning Prolonged targeted temperature management at 33°C did not result in better neurologic outcome; however, the study may have had limited power to detect clinically important differences, and further research may be warranted.

Hepatic encephalopathy update

From a recent review:

Hepatic encephalopathy is a state of brain dysfunction resulting from decompensation of cirrhosis. The mortality and morbidity associated with the overt form of hepatic encephalopathy are high, and even the covert form associates with poor outcomes and poor quality of life. We know that the dysfunction is not just an acute insult to the brain but rather results in long-standing cognitive issues that get worse with each episode of HE. Hence, there is an urgency to accurately diagnose these conditions, start appropriate therapy, and to maintain remission. Currently, we have two mainstay pharmacological treatment options (lactulose and rifaximin), but the narrative is evolving with new therapies under trial. Microbiome manipulation resulting in a favorable change to the gut microbiota seems to be a promising new area of therapy.

Troponin elevation in stroke: what does it mean?

From a recent study:

Background and Purpose—Acute ischemic stroke (AIS) patients may have raised serum cardiac troponin levels on admission, although it is unclear what prognostic implications this has, and whether elevated levels are associated with cardiac causes of stroke or structural cardiac disease as seen on echocardiogram. We investigated the positivity of cardiac troponin and echocardiogram testing within a large biracial AIS population and any association with poststroke mortality.

Methods—Within a catchment area of 1.3 million, we screened emergency department admissions from 2010 using International Classification of Diseases, Ninth Edition, discharge codes 430 to 436 and ascertained all physician-confirmed AIS cases by retrospective chart review. Hypertroponinemia was defined as elevation in cardiac troponin above the standard 99th percentile. Multiple logistic regression was performed, controlling for stroke severity, history of cardiac disease, and all other stroke risk factors.

Results—Of 1999 AIS cases, 1706 (85.3%) had a cardiac troponin drawn and 1590 (79.5%) had echocardiograms. Hypertroponinemia occurred in 353 of 1706 (20.7%) and 160 of 1590 (10.1%) had echocardiogram findings of interest. Among 1377 who had both tests performed, hypertroponinemia was independently associated with echocardiogram findings (odds ratio, 2.9; 95% confidence interval, 2–4.2). When concurrent myocardial infarctions (3.5%) were excluded, hypertroponinemia was also associated with increased mortality at 1 year (35%; odds ratio, 3.45; 95% confidence interval, 2.1–5.6) and 3 years (60%; odds ratio, 2.91; 95% confidence interval, 2.06–4.11).

Conclusions—Hypertroponinemia in the context of AIS without concurrent myocardial infarction was associated with structural cardiac disease and long-term mortality. Prospective studies are needed to determine whether further cardiac evaluation might improve the long-term mortality rates seen in this group.

Syncope review

Free full text.

Increased risk of stroke after an episode of sepsis

From a recent paper:

Background and Purpose—Infections have been found to increase the risk of stroke over the short term. We hypothesized that stroke risk would be highest shortly after a sepsis hospitalization, but that the risk would decrease, yet remain up to 1 year after sepsis.

Methods—This case-crossover analysis utilized data obtained from the California State Inpatient Database of the Healthcare Cost and Utilization Project. All stroke admissions were included. Exposure was defined as hospitalization for sepsis or septicemia 180, 90, 30, or 15 days before stroke (risk period) or similar time intervals exactly 1 or 2 years before stroke (control period). Conditional logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (95% CI) for the association between sepsis/septicemia and ischemic or hemorrhagic stroke.

Results—Ischemic (n=37 377) and hemorrhagic (n=12 817) strokes that occurred in 2009 were extracted where 3188 (8.5%) ischemic and 1101 (8.6%) hemorrhagic stroke patients had sepsis. Sepsis within 15 days before the stroke placed patients at the highest risk of ischemic (OR, 28.36; 95% CI, 20.02–40.10) and hemorrhagic stroke (OR, 12.10; 95% CI, 7.54–19.42); however, although the risk decreased, it remained elevated 181 to 365 days after sepsis for ischemic (OR, 2.59; 95% CI, 2.20–3.06) and hemorrhagic (OR, 3.92; 95% CI 3.29–4.69) strokes. There was an interaction with age (P=0.0006); risk of developing an ischemic stroke within 180 days of hospitalization for sepsis increased 18% with each 10-year decrease in age.

Conclusions—Risk of stroke is high after sepsis, and this risk persists for up to a year. Younger sepsis patients have a particularly increased risk of stroke after sepsis.

Septic encephalopathy

Free full text review.

P wave indices and risk of ischemic stroke

From a recent paper:

Conclusions—P-wave terminal force in lead V1, P-wave duration, and maximum P-wave area are useful electrocardiographic markers that can be used to stratify the risk of incident ischemic stroke.

Pseudo subarachnoid hemorrhage in post anoxic brain injury

Something to be aware of.

Review of motor neuron disease

With ALS as a prototype.

The relationship between atrial fibrillation and dementia

Reviewed in the green journal. It is unclear the extent to which it may be driven by factors other than stroke.

Longer sleep duration is associated with lower CRP levels

---in this study.

Spinal epidural abscess and diagnostic errors

From a recent report:

Abstract

Purpose

With this study, we set out to identify missed opportunities in diagnosis of spinal epidural abscesses to outline areas for process improvement.

Methods

Using a large national clinical data repository, we identified all patients with a new diagnosis of spinal epidural abscess in the Department of Veterans Affairs (VA) during 2013. Two physicians independently conducted retrospective chart reviews on 250 randomly selected patients and evaluated their records for red flags (eg, unexplained weight loss, neurological deficits, and fever) 90 days prior to diagnosis. Diagnostic errors were defined as missed opportunities to evaluate red flags in a timely or appropriate manner. Reviewers gathered information about process breakdowns related to patient factors, the patient–provider encounter, test performance and interpretation, test follow-up and tracking, and the referral process. Reviewers also determined harm and time lag between red flags and definitive diagnoses.

Results

Of 250 patients, 119 had a new diagnosis of spinal epidural abscess, 66 (55.5%) of which experienced diagnostic error. Median time to diagnosis in error cases was 12 days, compared with 4 days in cases without error (P less than .01). Red flags that were frequently not evaluated in error cases included unexplained fever (n = 57; 86.4%), focal neurological deficits with progressive or disabling symptoms (n = 54; 81.8%), and active infection (n = 54; 81.8%). Most errors involved breakdowns during the patient–provider encounter (n = 60; 90.1%), including failures in information gathering/integration, and were associated with temporary harm (n = 43; 65.2%).

Conclusion

Despite wide availability of clinical data, errors in diagnosis of spinal epidural abscesses are common and involve inadequate history, physical examination, and test ordering. Solutions should include renewed attention to basic clinical skills.

Sleep apnea update

This topic was reviewed in JACC. The full text is only available to subscribers but the audio summary is open access.

Here are a few points of interest:

Obstructive sleep apnea (OSA) is common in the general population.

Central sleep apnea (CSA) is largely confined to patients who already have cardiovascular disease, largely heart failure. It is particularly associated with heart failure with reduced ejection fraction. It is also associated with stroke and atrial fibrillation.

OSA is a cause of multiple cardiovascular disorders. CSA, though a result of certain cardiovascular disorders, can in turn contribute to further cardiovascular dysfunction, resulting in a vicious cycle of reciprocal cause and effect.

Although OSA is largely a disorder of obesity, in which fatty deposits in the upper airway are contributory, 20-30% of OSA is in non-obese individuals. In such cases upper airway dilator muscle dysfunction is believed to be at play.

Among the many consequences of sleep apnea are the metabolic effects of hypoxemia, increased sympathetic output, cytokine activation, endothelial dysfunction, insulin resistance, systemic and pulmonary hypertension and atrial fibrillation.

Treatment of OSA with CPAP ameliorates many of these, though treatment of CSA with positive pressure modalities has been disappointing and may be detrimental.

First, second and third generation cephalosporins cause delirium while cefepime and quinolones do not. Really?

I don’t believe this paper. Neither does Josh Farkas.