The patient with cirrhosis: poised to bleed or poised to clot?

It turns out to be a little of both. A number of reviews have addressed this. [1] [2] [3]  Here are some of the key points:

The old maxim that cirrhotic patients are auto-anticoagulated is a myth. Severe liver disease is associated with a delicate balance between bleeding and clotting. In general, cirrhosis tends to be a hypercoagulable state. The relative risk for VTE in such patients has been estimated at around 2.

 

What are the mechanisms for the hypercoagulability of liver disease?

In primary hemostasis, while platelet numbers are often decreased these platelets tend to be hyper-functional. This is due to low levels of ADAM TS 13, correspondingly increased levels of VW factor and multifactorial endothelial dysfunction.

In secondary hemostasis, reasons for hypercoagulability include decreased levels of liver dependent natural anticoagulants such as protein C, protein S, and antithrombin. Factor VIII (not synthesized in the liver) tends to be increased.

There is also impaired fibrinolysis with increased levels of PAI-1 and decreased levels of plasminogen.

What are the clinical implications?

Traditional hemostatic tests are generally used but are of limited reliability. There's been increasing interest in global hemostatic tests such as viscoelastic assays which are conceptually more valid but are not yet ready for translation into clinical practice.

For low risk procedures, prophylactic hemostatic products peri-procedure are generally not indicated.

Antithrombotic treatments should be given in accordance with standard clinical indications recognizing a potentially increased risk of bleeding.

DOACs can be used in many patients but certain published restrictions apply.

Special circumstances where warfarin is favored over DOACs

 When is warfarin favored over DOACs?

 Valvular atrial fibrillation. 

This term is becoming obsolete. For anticoagulation for stroke prevention in atrial fibrillation  DOACs are contraindicated and warfarin favored in severe rheumatic mitral stenosis and mechanical prosthetic valves.

Liver disease. 

If Child Pugh is C DOACs are not recommended. If B, apixaban and rivaroxaban can be used “with caution” (FDA labeling ).   Child Pugh calculator.

 Antiphospholipid syndrome. 

Warfarin is favored (Up to Date). 

Morbid obesity: 

DOAC is okay for BMI up to 40. Above 40 rivaroxaban and apixaban are acceptable but other DOACs should be avoided. 

History of gastrectomy or weight loss surgery: 

Warfarin preferred. This review summarizes the rationale and recommendations regarding morbid obesity and patients who have had weight loss surgery.

In addition, certain drug interactions with DOACs are category X thus prohibiting use.

ACC atrial fibrillation guidelines 2023

 A few key points from the 2023 atrial fibrillation guidelines American College of Cardiology

New classification: 

The old classification is maintained but it is encompassed in a broader classification outlining the stages of risk and /or the occurrence of atrial fibrillation. 

Stage 1:  at risk. This refers to the presence of risk factors such as obesity and hypertension. 

Stage 2: pre atrial fibrillation encompassing structural abnormalities such as LAE or warning arrhythmias such as  atrial ectopy.

Wiithin atrial fibrillation itself the traditional categories of paroxysmal persistent and permanent remain. Right above permanent atrial fibrillation is another designation referring to successful ablation. 

Flexibility is built into the CHA₂DS₂-VASc score for anticoagulation decisions. 

If the risk is intermediate there is considerable equipoise and shared decision making is advised. 

Increased preference for early rhythm control.

There is an increased emphasis on early rhythm control especially in patients with heart failure and reduced ejection fraction. Catheter ablation via pulmonary vein isolation now he has a class 1 indication particularly in patients with who present with heart failure and reduced ejection fraction at the time of the onset of atrial fibrillation detection.   Specifically:

Rhythm control recommended over rate control if decreased left ventricular function and persistent or high burden atrial fibrillation, class 1 

If atrial fibrillation is symptomatic, class 2a. 

Specific arrhythmias related to fibrillation have been defined. 

Atrial tachycardia is defined as a rate greater than or equal to 100, non sinus. Mechanisms can be automaticity, triggered or micro reentry  Atrial flutter. is considered any tachyarrhythmia  that involves macro re-entry. Typical flutter involves macro reentry that goes through the cavo tricuspid isthmus. All others are considered atypical.

Caffeine avoidance is noted not to be beneficial. 

The designation of valvular versus non-value or atrial fibrillation has become obsolete. 

The recommendation now is that for a mechanical prosthesis or severe rheumatic mitral stenosis warfarin is recommended.  DOACs are preferred for all other patients unless there are certain disease-related or pharmacokinetic contraindications. 

In cases of cryptogenic stroke there is a 2a recommendation for extended monitoring. The guidelines do not specify the duration of monitoring. 

For device detection of high rate episodes, (specifically pacemaker detection), stroke risk is believed to exist but believed to be less than that of clinical episodes. 

If a high rate episode is detected and lasts greater than or equal to 5 minutes it is almost always atrial fibrillation. For device detection of high rate episodes lasting greater than or equal to 24 hours systemic anticoagulation is given a 2a recommendation.   For the range of 5 minutes to 24 hours this same situation has a 2b recommendation. In both cases there is considered to be sufficient equipoise that shared decision making applies.

Atrial appendage occlusion devices such as the Watchman have a 2a recommendation if CHA₂DS₂-VASc  is greater than or equal to 2 and anticoagulation is contraindicated. 

For high bleeding risk but not a contraindication the device is given a 2b recommendation. 

There are some changes in systemic anticoagulation recommendations for varying degrees of kidney disease. 

Up to and including stage 3 systemic anticoagulation if otherwise recommended for atrial fibrillation has a class 1 recommendation. It drops to class 2a for stage 4 and to 2B if there is  esrg/hd. 

In atrial fibrillation with rheumatic valve disease or mechanical prosthesis for which vitamin K antagonist anticoagulation is recommended the CHA₂DS₂-VASc  score does not apply. 

The long-term rate control goal is an upper rate limit of 100-110 and has a 2a recommendation. 

Acute rate control

If EF is greater than 40, IV beta blocker or non-dihydropyridine calcium blocker, class 1.  Digoxin  if above ineffective or contraindicated class 2a. 

IV mag sulfate class 2a. It may be better than standard agents. Up to five grams is considered low dose. Occasionally one could use greater than or equal to 5 g.  The main use is adjunctive.

Amiodarone if others ineffective or contraindicated, class 2b.

AVN ablation indications

AV node ablation if rate control is refractory to medication and the patient is otherwise a candidate, 2a. This will be combined with pacing obviously and initial lower rate limit, to avoid malignant ventricular arrhythmia, should be set at 80 to 90 with plans to program down by monthly decrements of 10 until 60 is reached. 

 Stroke prevention associatied with cardioversion 

 If atrial fibrillation could have been going on greater than or equal to 48 hours 3 weeks of anticoagulation first or tee prior to cardioversion and anticoagulation for greater than or equal to 4 weeks afterwards. 

 Drugs to maintain sinus rhythm long-term. 

The guidelines are not very explicit about whether drugs should even be used in the first place. They merely say that such are “ reasonable “  for patients who are " not candidates for, or decline” ablation. Similarly those who prefer antiarrhythmic therapy to ablation are considered reasonable candidates. The implication is that you should probably do something to maintain sinus rhythm. 

If normal EF and no structural heart disease and no coronary disease then fleccanide or propofanone 2a

Dronedarone 2a if no recent decompensated HR and if HF class II or better.

Dofetilide 2a if no long QT or torsades risks and no hypokalemia or hypomag, or tendency thereto.

Amiodarone  is 2a but the agents above may be preferable. 

Sotalol is 2b with the same precautions that apply to dofetilide. 

In pts with prior MI, structural disease or EF less than or equal to 40% no recent decompensation or functional class III or worse, dronedarone is 2a.

When does antiarrhythmic therapy need to be administered in the hospital?  And for how long?

Dofetilide 3 d

Sotolol, admit to hospital but the guideline does not specify how long.

ICs:  Observe at least after the first dose.

PVI catheter ablation (pulmonary vein isolation ):

if antiarrhythmics not tolerated, contraindicated or not preferred, class 1.  For younger patients with no or few comorbidities class 1 as  first line even if the atrial fibrillation is paroxysmal. 

For atrial flutter, class 1 ( it would be implied that this is typical flutter ). For a new diagnosis of atrial fibrillation in heart failure with reduced ejection fraction both at the same time early rhythm control is class 1 and ablation is said to be “ beneficial when appropriate” class 1. 

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.

Primary aldosteronism: an update

 

Here's an update on this topic recently published in Cardiology in Review.

The original Conn syndrome was described in 1956 as a case report of a young woman with hypertension and severe hypokalemia who was found to have an adrenal adenoma and was cured after adrenalectomy. Subsequently we've found that primary aldosteronism is much more common than previously thought. It's certainly not a rare cause of secondary hypertension but it is markedly under-diagnosed.

The mechanism of action of aldosterone is described in the paper thusly:

Aldosterone, which is synthesized in the adrenal zona glomerulosa, acts primarily at the renal collecting tubule where it binds to mineralocorticoid receptors leading to an increased number of open epithelial sodium channels (ENaC) in the luminal membrane4 and increased Na-K-ATPase expression.5 Reabsorbed sodium leaves the luminal cell via the Na-K-ATPase pump. Subsequent intraluminal electronegativity triggers potassium secretion through membrane potassium channels. Additionally, aldosterone has been found to act at the second part of the distal convoluted tubule, where both the thiazide-sensitive sodium chloride cotransporter and ENaC are expressed. By regulating the function of these transporters, aldosterone is thought to have effects on sodium and chloride balance and blood pressure (BP) control.6

Hypokalemia is characteristic but only a minority of patients exhibit it at presentation.

Regarding the different etiologies, again, from the paper:

The most common cause of primary hyperaldosteronism is bilateral idiopathic hyperplasia (IHA), accounting for 60% of cases. An aldosterone-producing adenoma (APA) is seen in 30%, primary (unilateral) adrenal hyperplasia in 2%, aldosterone-producing adrenocortical carcinoma in less than 1%, familial hyperaldosteronism (FH) type 1 (glucocorticoid-remediable) in less than 1%, FH type 2 (APA or IHA) in less than 6%, and FH type 3 (germline KCNJ5 mutations) in less than 1%.9 Although germline mutations of KCNJ5 are quite rare, causing FH type 3 PA, somatic mutations of KCNJ5 are relatively common, and in one study was seen in 38% of patients with APA. These mutations are believed to increase expression of CYP11B2, the aldosterone synthase gene.10Glucocorticoid-remediable aldosteronism, which is inherited as an autosomal dominant trait, usually presents in childhood with moderate to severe hypertension. The pathophysiology involves ectopically synthesized aldosterone in the zona fasciculata under adrenocorticotropin control.

Patients with primary hyperaldosteronism have a higher cardiovascular risk then do those with comparable degrees of essential hypertension. This is believed to be due to direct extrarenal damaging effects of of aldosterone such as endothelial damage and myocardial fibrosis.

The two big questions are who should be screened and how to work it up. Guidelines are fairly aggressive in their recommendations for screening. They are covered in the paper. In brief, things that should trigger a workup include severity of hypertension (levels persistently exceeding 150 / 100), resistant hypertension which could be translated to mean failure to control the hypertension on 3 drugs or essentially any patient who is on four drugs even if controlled and hypokalemia whether spontaneous or diuretic associated. Additional candidates would include those with family history, those with early onset, and those with an adrenal incidentaloma. In addition those with sleep apnea are candidates. There is a somewhat poorly understood connection between sleep apnea and hyperaldosteronism.

It has been estimated that if these criteria or fully applied around 50% of hypertensive patients in primary care would be candidates for screening. This is straight out of of the Endocrine Society guidelines. This may seem like over testing and will certainly rule out the disorder in a substantial number of patients but it is promulgated in guidelines and published recommendations due to a substantially under-diagnosed disease burden.

Diagnosis starts with simultaneous measurement of renin and aldosterone. The renin measurement can either be plasma renin activity or renin concentration. Preferably these are done in the morning, seated for 5 to 15 minutes. The patient should be potassium and sodium replete and have diuretics discontinued. Unless the aldosterone to renin ratio is very high or spontaneous hypokalemia is observed further confirmatory testing is likely to be necessary followed by testing for the etiology of hyperaldosteronism. This includes ruling out glucocorticoid responsive hyperaldosteronism. Imaging is generally required followed often by adrenal vein sampling. Once one is past the initial screening test help from an endocrinologist or hypertension specialist might be warranted.

Anticoagulation for atrial fibrillation in stages 4 and 5 of CKD

From a recently published study:

Purpose

The aim of this study was to investigate whether oral anticoagulants can provide efficacy and safety profiles better than no anticoagulant in patients with stages 4 or 5 chronic kidney disease and atrial fibrillation.

Methods

From 2001 to 2017, a cohort of patients with stages 4 or 5 chronic kidney disease and atrial fibrillation based on electronic medical records were selected from Chang Gung Memorial Hospital system in Taiwan. Patients were divided into nonvitamin K antagonist oral anticoagulants (NOACs), warfarin, and nonanticoagulated groups. They were followed from the index date to the occurrence of the study outcomes or for 5 years, whichever occurred first. The outcomes were admissions due to ischemic stroke or systemic embolism or major bleedings. Survival analyses were conducted to estimate the incidence rates of outcomes.

Results

A total of 3771 patients with atrial fibrillation and estimated glomerular filtration rate less than 30 mL/min/1.73m 2 were enrolled, of whom 2971 were in the nonanticoagulated group, 280 in the NOAC group, and 520 in the warfarin group. About 25% of all subjects (940 patients) were on dialysis. The mean follow-up was 3.2 years. After adjusting for sex, age, comorbidities, and comedication, the warfarin group had a significantly higher risk of ischemic stroke or systemic embolism (adjusted hazard ratio [aHR] 3.1, 95% confidence interval [CI] 2.1-4.6) than the nonanticoagulated group. The NOAC group had a similar risk of ischemic stroke or systemic embolism (aHR 1.1; 95% CI 0.3-3.4) to that of the nonanticoagulated group. Both the warfarin and the NOAC groups had a significantly higher major bleeding risk than the noncoagulated group (aHR 2.8 [95% CI 2.0-3.8] for warfarin; aHR 3.1 [95% CI 1.9-5.2] for NOAC).

Conclusion

The use of NOACs or warfarin is not more effective than using no anticoagulants at all in reducing the risk of ischemic stroke or systemic embolism. Both NOACs and warfarin are associated with increased risk of major bleeding. Our results do not support the use of anticoagulants in patients with atrial fibrillation and stages 4-5 chronic kidney disease.

From an accompanying editorial:

The present study makes a significant contribution to the controversial field of oral anticoagulation in chronic kidney disease patients and advises against an unselected anticoagulant treatment of elderly chronic kidney disease stages 4-5 patients with atrial fibrillation to prevent thromboembolic events. Physicians are again left with an individualized approach to these patients weighing carefully in the inherent benefits and risks of oral anticoagulation.

Elevated BP in hospitalized patients: what to do?

From a recently published review:

Elevated blood pressure is common in patients who are hospitalized. There are no guidelines and few recommendations to help inpatient providers manage patients with elevated blood pressure. There are no normal reported values for blood pressure in the inpatient and recording circumstances often widely vary. Many factors may influence blood pressure such as pain, anxiety, malaise, nicotine withdrawal, or withholding home medications. This review of available literature suggests potential harm and little to no potential benefit in treating asymptomatic patients with elevated blood pressure. This review also found no evidence that asymptomatic elevated blood pressure progresses to lead to end-organ damage. However, there are clear instances of hypertensive emergency where treatment is indicated. Conscientious adjustment of an anti-hypertensive regimen should be undertaken during episode of elevated blood pressure associated with end-organ damage.

Cardiac complications of psoriasis

Look at the epicardial fat. From a recent paper in the green journal:

Psoriasis is a systemic inflammatory disorder that can target adipose tissue; the resulting adipocyte dysfunction is manifest clinically as the metabolic syndrome, which is present in ≈20%-40% of patients. Epicardial adipose tissue inflammation is likely responsible for a distinctive pattern of cardiovascular disorders consisting of 1) accelerated coronary atherosclerosis leading to myocardial infarction, 2) atrial myopathy leading to atrial fibrillation and thromboembolic stroke, and 3) ventricular myopathy leading to heart failure with a preserved ejection fraction. If cardiovascular inflammation drives these risks, then treatments that focus on blood pressure, lipids, and glucose will not ameliorate the burden of cardiovascular disease in patients with psoriasis, especially in those who are young and have severe inflammation. Instead, interventions that alleviate systemic and adipose tissue inflammation may not only minimize the risks of atrial fibrillation and heart failure but may also have favorable effects on the severity of psoriasis. Viewed from this perspective, the known link between psoriasis and cardiovascular disease is not related to the influence of the individual diagnostic components of the metabolic syndrome.

Updated atrial fib guidelines: the essentials

 

From Joseph S.Alpert.

The cholesterol hypothesis is alive again!

From a recent paper in JAMA:

Key Points

Question Is consuming dietary cholesterol or eggs associated with incident cardiovascular disease (CVD) and all-cause mortality?

Findings Among 29 615 adults pooled from 6 prospective cohort studies in the United States with a median follow-up of 17.5 years, each additional 300 mg of dietary cholesterol consumed per day was significantly associated with higher risk of incident CVD (adjusted hazard ratio [HR], 1.17; adjusted absolute risk difference [ARD], 3.24%) and all-cause mortality (adjusted HR, 1.18; adjusted ARD, 4.43%), and each additional half an egg consumed per day was significantly associated with higher risk of incident CVD (adjusted HR, 1.06; adjusted ARD, 1.11%) and all-cause mortality (adjusted HR, 1.08; adjusted ARD, 1.93%).

Meaning Among US adults, higher consumption of dietary cholesterol or eggs was significantly associated with higher risk of incident CVD and all-cause mortality in a dose-response manner.

This paper has been wildly overhyped. It’s new data but concludes nothing we didn’t already know: cholesterol matters. The real problem is, so do a lot of other things. Those who would hype this finding lack an appreciation of the concept of population attributable risk.

Which patients post cardiac arrest need to go straight to the cath lab?

From a recent AHA scientific statement:

CAD is a common substrate, and its severity is a potential trigger for OHCA, especially in the case of shockable rhythms. Patients with VF/pVT OHCA should be considered at the highest severity of a continuum of acute coronary syndromes. Patients with VF/pVT have a significant burden of CAD: acute, chronic, or acute on chronic (Figure 8)…

Current guidelines recommend early CAG and reperfusion for postarrest patients manifesting ST-segment elevation after ROSC is achieved. However, because of a lack of conclusive randomized data and ongoing perceived clinical equipoise, there is no consensus guideline on the use of CAG and coronary revascularization in patients without ST-segment elevation on ECG. Multiple randomized trials addressing this question are underway. Until their completion, there is a significant body of observational studies that address the role of the CCL in this population.

The current evidence suggests that early access to the CCL in patients resuscitated from VF/pVT cardiac arrest is associated with 2- to 3-fold higher functionally favorable survival rates than more conservative approaches of late or no access to the CCL. This body of evidence, with potential for unmeasured selection bias, suggests that patients resuscitated from OHCA, especially those with presenting shockable rhythms, should be considered for early CAG, identification of reversible causes, and revascularization when indicated.

This is in line with the current ACLS guidelines, which say that if there’s ST elevation post ROSC an immediate trip to the cath lab carries a class I recommendation. For patients without STE, the guidelines give a IIa recommendation to go straight to the cath lab if the arrest is of suspected cardiac origin on clinical grounds.

Cardiorenal syndrome

The AHA scientific statement is available as free full text here.

Rates of cardiac testing prior to hip fracture surgery

From a recent report:

Hip fracture is a common reason for urgent inpatient surgery. In the past few years, several professional societies have identified preoperative echocardiography and stress testing for noncardiac surgeries as low-value diagnostics. We utilized data on hospitalizations with a primary diagnosis of hip fracture surgery between 2011 and 2015 from the State Inpatient Databases (SID) of Maryland, New Jersey, and Washington, combined with data on hospital characteristics from the American Hospital Association (AHA). We found that the rate of preoperative ischemic testing is surprisingly but encouragingly low (stress tests 1.1% and cardiac catheterizations 0.5%), which is consistent with studies evaluating the outpatient utilization of these tests for low- and intermediate-risk surgeries. The rate of echocardiograms was 12.6%, which was higher than other published reports. Our findings emphasize the importance of ensuring that quality improvement efforts are directed toward areas where quality improvement is, in fact, needed.

A fib ablation vs antiarrhythmic medication

From a recent study published in JAMA, the CAPTAF trial:

Key Points

Question Is pulmonary vein isolation more effective than optimized antiarrhythmic drug therapy for improving general health in patients with symptomatic atrial fibrillation?

Findings In this randomized clinical trial that included 155 patients with paroxysmal or persistent symptomatic atrial fibrillation despite use of antiarrhythmic medication, the improvement in quality of life at 12 months for those treated with catheter ablation compared with antiarrhythmic medication was 11.9 vs 3.1 points on the 0- to 100-point 36-Item Short-Form Health Survey questionnaire, a difference that was statistically and clinically significant.

Meaning In patients with either paroxysmal or persistent symptomatic atrial fibrillation despite medication, catheter ablation may help improve quality of life.

Abstract

Importance Quality of life is not a standard primary outcome in ablation trials, even though symptoms drive the indication.

Objective To assess quality of life with catheter ablation vs antiarrhythmic medication at 12 months in patients with atrial fibrillation.

Design, Setting, and Participants Randomized clinical trial at 4 university hospitals in Sweden and 1 in Finland of 155 patients aged 30-70 years with more than 6 months of atrial fibrillation and treatment failure with 1 antiarrhythmic drug or β-blocker, with 4-year follow-up. Study dates were July 2008–September 2017. Major exclusions were ejection fraction less than 35%, left atrial diameter greater than 60 mm, ventricular pacing dependency, and previous ablation.

Interventions Pulmonary vein isolation ablation (n = 79) or previously untested antiarrhythmic drugs (n = 76).

Main Outcomes and Measures Primary outcome was the General Health subscale score (Medical Outcomes Study 36-Item Short-Form Health Survey) at baseline and 12 months, assessed unblinded (range, 0 [worst] to 100 [best]). There were 26 secondary outcomes, including atrial fibrillation burden (% of time) from baseline to 12 months, measured by implantable cardiac monitors. The first 3 months were excluded from rhythm analysis.

Results Among 155 randomized patients (mean age, 56.1 years; 22.6% women), 97% completed the trial. Of 79 patients randomized to receive ablation, 75 underwent ablation, including 2 who crossed over to medication and 14 who underwent repeated ablation procedures. Of 76 patients randomized to receive antiarrhythmic medication, 74 received it, including 8 who crossed over to ablation and 43 for whom the first drug used failed. General Health score increased from 61.8 to 73.9 points in the ablation group vs 62.7 to 65.4 points in the medication group (between-group difference, 8.9 points; 95% CI, 3.1-14.7; P = .003). Of 26 secondary end points, 5 were analyzed; 2 were null and 2 were statistically significant, including decrease in atrial fibrillation burden (from 24.9% to 5.5% in the ablation group vs 23.3% to 11.5% in the medication group; difference –6.8% [95% CI, –12.9% to –0.7%]; P = .03). Of the Health Survey subscales, 5 of 7 improved significantly. Most common adverse events were urosepsis (5.1%) in the ablation group and atrial tachycardia (3.9%) in the medication group.

Conclusions and Relevance Among patients with symptomatic atrial fibrillation despite use of antiarrhythmic medication, the improvement in quality of life at 12 months was greater for those treated with catheter ablation compared with antiarrhythmic medication. Although the study was limited by absence of blinding, catheter ablation may offer an advantage for quality of life.

Syncope guidelines

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

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.

Appropriateness of troponin ordering in the hospital

Form a recent study:

Troponin assays are integral to the diagnosis of acute myocardial infarction (AMI), but there is concern that testing is over utilized and may not conform to published guidelines. We reviewed all testing performed at 14 hospitals over 12 months and associated troponin values with the primary and secondary diagnoses for each visit. Troponin was determined to be negative, indeterminate or elevated based on reference ranges. The majority of troponin measurements were single, not serial (64%). The rate of AMI was low, with only 3.5% of tested patients having a primary or secondary diagnosis of AMI. Sensitivity, specificity and negative predictive value were excellent, exceeding 90%. However, positive predictive value was low, suggesting testing of populations with diseases known to be associated with elevated troponin levels in the absence of AMI. The majority (79%) of elevated troponin values were associated with primary diagnoses other than AMI. Only 28% of elevated troponins were associated with a primary or secondary diagnosis of AMI. These data suggest possible overuse of troponin testing in our healthcare system. Journal of Hospital Medicine 2017;12:329-331. © 2017 Society of Hospital Medicine

This conclusion is premised on the idea that the only reason to order a troponin is to diagnose or exclude MI.

Vitamin C deficiency as a cause of pulmonary hypertension

A dramatic case report of this previously known entity.

Hospitalization rates and lengths of stay for VTE in Alberta Canada

Since 2002 they have been sending a fair number of patients home from ER or clinic but once hunkered in patients stay awhile and these numbers haven’t changed much over time:

 

Background

Acute venous thromboembolism leads to significant morbidity and mortality. Advances in pharmacotherapy facilitate outpatient care in low-risk acute venous thromboembolism. The proportion of hospitalized acute venous thromboembolism cases and the average length of stay are not known. We sought to identify predictors of hospitalization, changes in hospitalization rates and length of stay of acute venous thromboembolism over a decade in Alberta, Canada.

Methods

Using linked administrative health databases, we identified adult patients diagnosed primarily with acute venous thromboembolism between April 2002 and March 2012. We measured trends using Poisson regression, adjusted length of stay using analysis of covariance. We identified predictors of hospitalization using multivariate logistic regression.

Results

8198 out of 31,656 acute venous thromboembolism cases were hospitalized. The overall venous thromboembolism admission rates ranged between 23.7% and 27.8% with no evident temporal trend (P = 0.10). The average admission rate was 51.9% for pulmonary embolism and 16.1% for deep vein thrombosis. The mean length of stay for deep vein thrombosis and pulmonary embolism remained unchanged with an adjusted mean for venous thromboembolism of 6.9 ± 1.0 days. Higher Charlson index, older age, male gender, pulmonary embolism at presentation and multiple comorbidities were associated with hospitalization. Hospitalization was associated with 30-day mortality (odds ratio:2.8, 95% CI: 2.2–3.5) whereas the length of stay was not (odds ratio:1.0, 95% CI: 0.99–1.0).

Conclusion

Hospitalization rates and mean length of stay for acute venous thromboembolism did not change significantly between 2002 and 2012. Advances in pharmacotherapy have not yet reduced hospitalization rates or length of stay for venous thromboembolism.