Not only can it be useful in identifying those with history of dizziness upon standing but it may also predict a higher risk of falls, fracture, syncope and mortality long term. 1
Clinicians (myself included) have often assumed that drops in blood pressure (BP) and brief feeling of light-headedness soon after active standing are too common and “physiologic” to be of clinical utility,1,2 and have often discouraged checking for orthostatic hyotension (OH) sooner than 1 minute.
However, a 2017 report involving over 11,000 middle-aged participants (Atherosclerosis Risk in Communities Study) may make us rethink our position.1 This prospective study found a significant association between participant-reported history of dizziness on standing and OH (defined as a drop in BP systolic ≥20 mmHg or diastolic ≥10 mmHg) but only at 1st measurement (mean of 28.0 seconds after standing), not at subsequent ones over a 2 minute period.
The more intriguing finding was the association between OH documented < 1 minute after standing and increased risk of falls, fracture, syncope, and mortality over a median follow-up period of 23 years. Although there were limitations to the study (eg, excluding many patients likely to have more severe OH), it appears that “premature” checking for OH less than a minute after standing may not be useless!
Most, including the CDC, agree that rechecking the BP at 3 minutes is still indicated to identify those with sustained or delayed OH. 2,3
Also go to a related P4P post: https://pearls4peers.com/2015/12/14/how-can-i-be-sure-that-my-patient-truly-has-orthostatic-hypotension-oh/
- Juraschek SP, Daya N, Rawlings AM, et al. Comparison of early versus late orthostatic hypotension assessment times in middle-age adults. JAMA Intern Med 2017;1177:1316-1323. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5661881/
- Singer W, Low PA. Early orthostatic hypotension and orthostatic intolerance-more than an observation or annoyance. JAMA Intern Med 2017;1177:1234-25. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2645144
- CDC. https://www.cdc.gov/steadi/pdf/measuring_orthostatic_blood_pressure-a.pdf. Accessed February 7, 2017.
It depends on the timing of your patient’s presentation!
It is generally held that serum prolactin level peaks within 10-20 min after a generalized tonic-clonic or complex partial seizure and returns to baseline within 2-6 h. Even then, its sensitivity is no more than 50%-60% for these types of seizures. Elevated PL is also seen in 60%-80% of patients with syncope.1
A report by the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology (2006) concluded that “elevated serum prolactin assay, when measured in the appropriate clinical setting at 10-20 min after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic non-epileptic seizure among adults or older children (Level B).2
In contrast, reports of PL increasing for up to 6 h after epileptic seizure or not reaching baseline for 12-18 h can also be found in the literature.3
Although the mechanism for elevation of PL in certain seizures is unknown, one hypothesis proposes that prolactin is secreted due to the interference with the inhibitory control of hypothalamus by the electrical perturbation of this part of the brain.4
- Nass RD, Sassen R, Elger CE. The role of postictal laboratory blood analyses in the diagnosis and prognosis of seizures. Seizure 2017;47:51-65. https://www.ncbi.nlm.nih.gov/pubmed/28288363
- Chen DK, So YT, Fisher RS. Is prolactin a clinically useful measure of epilepsy? Epilepsy Currents 2006;6:78-79. https://www.ncbi.nlm.nih.gov/pubmed/16157897
- Siniscalchi A, Gallelli L, Mercuri NB, et al. Serum prolactin levels in repetitive temporal epileptic seizures. Eur Rev Med Pharmacol Sci 2008;12:365-368. https://www.ncbi.nlm.nih.gov/pubmed/19146198
- Collins WCJ, Lanigan O, Callaghan N. Plasma prolactin concentrations following epileptic and pseudoseizures. J Neurol Neurosurg Psych 1983; 46:505-8. http://jnnp.bmj.com/content/jnnp/46/6/505.full.pdf
Yes, conduction abnormalities, particularly left bundle branch block (LBBB), frequently complicate transcatheter aortic valve replacement (TAVR).
A 2016 systematic review and meta-analysis reported new-onset LBBB following TAVR and persisting at hospital discharge in 13.3%-37% of patients1; the incidence may be higher or lower depending on the type of prosthesis used.2,3 In the same systematic review, new-onset LBBB was associated with a higher risk of permanent pacemaker placement (PPI) and cardiac death during 1-year followup. In another study, persistence of LBBB post-TAVR without PPM placement was associated with an increased risk of syncope, complete AV node block, and PPI, but not overall mortality.4
The underlying anatomy of the conduction system may help explain post-TAVR conduction complications. The AV node is located adjacent to the membranous septum, closely associated with the subaortic region and LV outflow track, giving rise to the LBB.5 Protrusion of TAVR prostheses into the LV outflow tract, the mechanical injury occurring during the predilation or the positioning of the valve, and potential trauma to the conduction system by the catheters and guidewires used in TAVR may all contribute to these complications.3,5
- Regueiro A, Altisent OA, Del Trigo M, et al. Impact of new-onset left bundle branch block and periprocedural permanent pacemaker implanation on clinical outomces in patients undergoing transcatheter aortic valve replacement: A systematic review and meta-analysis. Circ Cardiovasc Interv 2016;9:e003635. http://circinterventions.ahajournals.org/content/9/5/e003635.long
- Nazif, T.M., Williams, M.R., Hahn, R.T., Kapadia, S., Babaliaros, V. et al. Clinical implications of new-onset left bundle branch block after transcatheter aortic valve replacement: analysis of the PARTNER experience. Eur. Heart J. 2014;21:1599-1607. https://www.ncbi.nlm.nih.gov/pubmed/24179072
- Bourantas CV, Serruys PW. Evolution of transcatheter aortic valve replacement. Circ Res 2014;114:1037-1051. http://circres.ahajournals.org/content/114/6/1037
- Urena, M., Mok, M., Serra, V., Dumont, E., Nombela-Franco, L. et al. Predictive factors and long-term clinical consequences of persistent left bundle branch block following transcatheter aortic valve implantation with a balloon-expandable valve. J Am Coll Cardiol. 2012;60:1743-1752. https://www.ncbi.nlm.nih.gov/pubmed/23040577
- Piazza, N., Jaegere, P., Schultz, C., Becker, A.E., Serruys, P.W., Anderson, R.H. Anatomy of the aortic valve complex and its implications for transcatheter implantation of the aortic valve. Circ Cardiovasc Interv. 2008;1:74-81. https://www.ncbi.nlm.nih.gov/pubmed/20031657
Contributed by Salvatore D’Amato MD, Mass General Hospital, Boston, MA
Syncope is a well-known initial manifestation of pulmonary embolism (PE)1. However, given the varied causes of syncope, determining the prevalence of PE among patients hospitalized for syncope is important.
A recent NEJM study furthers our understanding of PE and syncope2. This multicenter prospective study enrolled 560 patients not already on anticoagulation who were hospitalized for a first episode syncope. Of 230 patients who had either a high pretest probability for PE, positive D-dimer assay or both, PE was diagnosed in 97 (17%, or nearly 1 of 6 of enrolled patients) based on CT or ventilation/perfusion scan. PE was found more frequently among patients with syncope of undetermined cause than those with an alternative explanation (25.4% vs 12.7%).
The results of this study should make us consider, perhaps more frequently, the possibility of PE in patients hospitalized for first episode syncope not on anticoagulants, particularly those without an alternative explanation.
- Thames MD, Alpert JS, Dalen JE. Syncope in patients with pulmonary embolism. JAMA 1977;238:2509-2511. https://www.ncbi.nlm.nih.gov/pubmed/578884
- Prandoni P, Lensing AWA, Prins MH, et al. Prevalence of pulmonary embolism among patients hospitalized for syncope. N Engl J Med 2016;375:1524-31. http://www.nejm.org/doi/full/10.1056/NEJMoa1602172
Contributed by Rebecca Berger MD, Department of Medicine, Mass General Hospital, Boston, MA.
Although we often think of syncope caused by PE in the setting of right ventricular failure and shock, less serious PE can also cause syncope by triggering a vaso-vagal reflex as supported by several case reports (1). Further supporting the potential role of neurogenic cause of syncope in at least some cases of PE is a study demonstrating that patients with syncope as a presenting symptom of PE did not show a more serious clinical picture (e.g. shock) than those without syncope (1). In another study of the clinical presentation of acute PE, EKG signs of acute right ventricle overload was found in only 25% of patients with syncope (2). So we shouldn’t rule out PE as cause of syncope just because signs of hemodynamic compromise are absent.
1. Castelli R, Tarsia P, Tantardini G et al. Syncope in patients with pulmonary embolism: comparison between patients with syncope as the presenting symptom of pulmonary embolism and patients with pulmonary embolism without syncope. Vascular Medicine 2003;8:257-261.
2. Miniati M, Cenci, Monti S, et al. Clinical presentation of acute pulmonary embolism: survey of 800 cases. PloS One 2012;7:e30891.