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Archive for May, 2021

No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  

 

Reference

1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 

 

 

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Here is an uncommon story of a patient with palpitation,SVT , Troponin +ve, and suspected ACS.

Palpitation in ER ⇒ {Tachycardia +Troponin positive ≠ ACS}

Mechanism of troponin elevation following any SVT

  • At high heart rates (>200) myocardium is subjected to non-Ischemic mechanical strain & squeeze. Minute amounts of Troponin is let out like a myocardial juice into the circulation (Like atrial natriuretic peptide release which causes polyuria during AVNRT)
  • Tropinin releases have been shown to correlate with both heart rate and duration of ST depression (Subendocardial strain /AVRT left lateral pathways)
  • Short diastole induced low coronary perfusion pressure and a true transient (but insignificant) Ischemia
  • Finally, SVT (especially in the elderly) is a natural “exercise stress test” equivalent, ST depression with Troponin positivity is a true marker of significant epicardial CAD

Significance

False alarm of ACS is the most important issue. (Except one study which showed a different conclusion Chow GV, Prognostic significance of cardiac troponin I level in hospitalized patients presenting with supraventricular tachycardia. Medicine (Baltimore) 2010;89:141–148. doi: 10.1097/MD.0b013e3181dddb3b. [PubMed]

Note: If AVNRT occurs with aberrancy, or AVRT presents as antidromic tachycardia with a wide qrs tachycardia the confounding effect is perfect as it can no way be differentiated from true Ischemic VT or atrial fibrillation.

Final message

It is no ER room secret that a single spot Troponin value has lost its credibility considerably in segregating ACS from non-ACS conditions. It is falsely elevated in a long list of cardiac and noncardiac conditions. It is a worthy point of learning, among the cardiac conditions, the commonest cause for false elevation is during any tachycardia. This should be kept in mind. Because a patient with chest pain who present with benign palpitation due to prior SVT (Arrival ECG could be normal) a false raise can trigger a chain of inappropriate reaction that may land the spot even in the cath lab.

Postample

In spite of these limitations, non-diagnostic ECGs, we expect Troponin and CPK to guide us in chest pain screening. We now have added one more marker, high sensitivity Troponin Assays. Let us believe, it doesn’t add to more confusion. I think the main purpose of these biomarkers in the future, would be to arrest the habit of using cath lab as triaging place for chest pain instead of ER room. (A brief review from ACC https://www.acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians)

Reference

1.Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Ben Yedder N, Roux JF, Paredes FA Can J Cardiol. 2011 Jan-Feb; 27(1):105-9. [PubMed] [Ref list]

2.Kanjwal K, Imran N, Grubb B, Kanjwal Y. Troponin elevation in patients with various tachycardias and normal epicardial coronaries. Indian Pacing Electrophysiol J. 2008;8(3):172-174. Published 2008 Aug 1.
3.Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med. 2011;29:545–548. doi: 10.1016/j.ajem.2010.01.041. [PubMed] [CrossRef] []

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