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Archive for the ‘cardiology research topics for fellows’ Category

The branching pattern of the human cardio-vascular tree is as unique as one’s fingerprint. One such hugely variable anatomy is the SA nodal blood supply.

Certain salient features

  • Variation can be seen in origin, course, and termination.
  • Now it is estimated to arise from RCA in 70% (Moved up from 55% in old studies )
  • From LCX (25%)
  • Dual SA node supply(5%)
  • Direct from Aorta

It is heartening to find this good anatomical review on this topic.

A) From the Right Coronary Artery; (B) From the Left Circumflex Artery (proximal); (C) From the Left Circumflex Artery (distal); (D) From the Left Coronary Artery; (E) From the Aorta; (F) Dual origin from the Right Coronary Artery and the Left Circumflex Artery. Image source : Vikse J, PLoS ONE 11(2): e0148331

Implication for the surgeon

The whereabouts of this tiny, yet important artery is critical to the surgeons’ as they incise and explore the atrial roof. (A gateway, that gives access to so many cardiac surgeries) The SA nodal artery mostly goes retro caval but it can be peri-caval or even anterior to SVC.

This image shows (a,b,c) the course in relation to SVC, Developmentally as the venous pole go posteriorly to fix the SA artery behind it.Image source : Vikse J, PLoS ONE 11(2): e0148331

For the Interventional cardiologist

A rare but distinct mechanical compression of SA node artery is reported with large ASD closure device. The plane of compression is usually occurring in the superior aspect of IAS when the SA node artery cross over the RA to reach the SA node. Should be suspected whenever unusual bradycardia occurs during the manipulation of the device or just after deployment. Always mind the delicate gap  between the antero superior rim and disc where SA nodal artery is likely to trespass.

AV node Ischemia with ASD device

With precise imaging modalities, new secrets are emerging. Additional AV node arteries from proximal RCA is documented.This is a surprising learning point for us. This artery is referred to as the right superior descending artery, which provides an alternative blood supply to the AV node from the proximal right coronary artery. The transient compromise of this hitherto unknown AV nodal twigs by the ASD device cause AV blocks. With this new info, we also got an answer to one more lingering question, why would disproportionate bradycardias are observed in inferior MI even when distal RCA is flowing well. We can’t blame high vagal tone always.

SA node compression by ASD device amplatzer

A CT angiogram showing how the ASD device encroaches the SA node artery. Image Source:Tsunehisa Yamamoto JACC 2016 (Linkedbelow)

The original article has an excellent video clipping of how an ASD device hugs the SA node at the superior edge of ASD.

Final message

Human anatomy is not the subject meant to be read in the first-year medical school cadavers, & forget thereafter. Surprisingly. the field of anatomy is also evolving with new mysteries exposed by modern imaging.SA nodal arterial blood supply is one such interesting aspect of cardiac anatomy. Young fellows in cardiology shall pursue further anatomical dark spaces in the heart (One such topic is how cardiac lymphatics compete with the venous system in draining cardiac interstitium)

Reference

Vikse J, Henry BM, Roy J, RamakrishnanPK, Hsieh WC, Walocha JA, et al. (2016) AnatomicalVariations in the Sinoatrial Nodal Artery: A Meta-Analysis and Clinical Considerations. PLoS ONE 11(2): e0148331

It’s gratifying a unique and committed group exclusively doing research in Anatomy. It Department of Anatomy, Jagiellonian University Medical College, Krakow Poland.

http://www.eba.cm.uj.edu.pl/

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In CKD, LVH is a near-constant feature with echo showing thick, bright echoes from IVS. The LV mass increases, partly due to physiological hypertrophy ,also contributed by deposits of uremic middle molecules and fluid collection in the interstitium as myocardial edema.This, is recognised as T 2 weighted MRI signals. Chronic fluid stasis may progress to myocardial fibrosis. (Kidney Blood Press Res 2018;43:134–142 )  

Effect of Frusemide on myocardial edema 

We know, loop diuretics cause aggressive depletion of ECF volume and to a lesser extent Interstitial fluid. The effect of diuretic on myocardial water content is a poorly studied parameter.(Still more visible to a shrewd echocardiographer)

Effect of dialysis

While the effect of diuretics on myocardial edema is not consistent, however, we have observed definite regression of myocardial thickness, mass, and rigidity following dialysis. This transforms into a better LV systolic and diastolic function. At least in one patient, we have observed  the E velocity shrunk more than 50% the next day following dialysis pushing them to lower grades of HFpEF( A potential study topic.)

Final message 

The Improvement of the functional class of CKD patients immediately after dialysis is not only attributable to the removal of excess fluid and toxic uremic molecules, regression of myocardial edema plays an important role.

Further reading

Trinh E, Chan C, T: Intensive Home Hemodialysis Results in Regression of Left Ventricular Hypertrophy and Better Clinical Outcomes. Am J Nephrol 2016;44:300-307.

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