- At any branch point three angles are possible .True bifurcation angle is formed between LAD and LCX .
- The angle between LM and LAD or LM and LCX can also be important in specific situations ,especially when we encounter short left mains and Medina 1,1,0 lesions .
- Major bifurcation angle can occur in mid segments as well , between LAD / major Diagonal , LCX and OM.
- Logic would tell us the left main bifurcation angle is relatively fixed by the anatomical AV and IV grooves. Still early course of LAD and LCX can be out of grooves.
- Further ,the bifurcation angle is imparted some amount of dynamism by cardiac cycle . It can vary between 80 -120 degrees (LAD/LCX).
- Most importantly various angiographic views can alter the true angle (by illusion ) in dramatic fashion . RAO caudal view appear ideal to measure it. (LAO caudal make every bifurcation angle obtuse !)
- Acute angled bifurcations are prone for stent related mechanical issues both during deployment and in the long term outcome . (When two stent technique is used) This is because , acute angled bifurcations has a tendency to drift the carina , and encroach the lumen which can create new turbulence . Of course final kissing balloon is expected to reduce this hemodynamic side effect at least on paper !
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, cath lab tips and tricks | Tagged bifurcation lesion, bifurcation pci, carina plaque shift bifurcation lesion, medina classification, true bifurcation angle | Leave a Comment »
Modern men think they are invincible . They can innovate every thing under the sun with their sixth sense . Alas . . . we forget human values ! .It does not require a least of that special sense . Reaching out to a life in distress require an animal sense !

The Antics ! Crossing a bridge with fifth sense ! The Hindu 5th April 2013 Image : Michale Nongthombam.
A bunch of Ants plan how to ferry a daughter Ant , across a broken bridge and execute it efficiently with their tiny little cerebrum !
While , we boast around with the later . . . still . . . there is no end in sight for all those self inflicted sufferings . . . these lesser mortals live happily in this human infested planet !
Posted in bio ethics, medical quotes | Tagged commmon sense in medicine, ethics in modern science, fith sense vs sixth sense, great photographs in animals, human sense and animal sense, wild life photography | 1 Comment »
Have you ever wondered a given chest x-ray is taken in systole or diastole ? We should . . . isn’t ? Statistically chances of a X ray to fall in diastole is 10-20 % more than systole as the later phase is longer . The peculiarity of cardiac anatomy is that , the profile of the heart alters so little between systole and diastole .Still the blood is pumped efficiently into both pulmonary and systemic circulation . The left ventricle shortens by 35% and ejects 65 % of blood . Similarly RV shortens but with lesser quantum.
In a simple and elegant study by Stephen Gammill in 1970 published in Radiology journal,
he concluded the following about the CT ratio between systole and diastole.
- 52 % showed changes of 0.3 cm
- 41 per cent showed alterations of 0.4 to 0.9 cm,
- Only 7 per cent showed a significant variation of 1.0 to 1.7 cm in transverse cardiac diameter.
(I wonder why any follow up studies on this vital issue is scarce !)

In spite both ventricles contracting during systole the radiological transverse cardiac diameter is relatively undisturbed !
Importance of Rotary , Twist ,Torsional and Longitudinal motion
The fact that CT ratio does not alter significantly in most , imply the heart has some other kinetic motion which does not compromise the transverse diameter during systole. They are the rotary , and twist motion .The relative constancy of CT ratio is a good evidence for existence for such alternate motions .We have since confirmed this by sophisticated echocardiographic techniques .
Another evidence for rotary motion recognised in the bed side when the apical impulse hits you in the fingers even as the ventricle is supposed to go away from chest wall during systole . This is the torsional movement of LV apex and adjacent inter ventricular septum .
Reference
http://radiology.rsna.org/content/94/1/115.abstract
Coming soon
Inspiratory and expiratory x ray chest and the effect on cardiac contours .
Posted in cardiac radiology, Cardiology -unresolved questions | Tagged ct ratio during systole and diastole, transverse cardiac diameter and systole and diastole, what is the effect of cardiac contractility on ct ratio ? |
In the early 1980s , when cardiac physicians were confronting how to tackle intra coronary thrombus , one man from Japan was looking directly at the ground zero with fiber-optic coronary angioscope .He provided live images of coronary plaques and thrombus (long before the IVUS and OCT era) because of technical difficulties it did not get into clinical utility but gave us vital information like plaque morphology and behavior.
- The concept of red and white thrombus
- The yellow lipid enriched vulnerable plaques
- Post lytic clot surface
- The fibrin strands within the clot etc.
The angioscopes have now given way to IVUS and OCT which provide indirect vision of the coronary arteries .Uchida has written a book tilted coronary angioscaopy which is a must read for all clinical cardiologists.
I think Japanese are leading in this aspect of cardiac Imaging .Yasunori Ueda is another person who has done lot of work on angioscopy . here is an Image from his paper. Exciting stuff is isn’t !

Image source : Yasunori Ueda http://www.invasivecardiology.com
Reference
Posted in Cardiology -Interventional -PCI, Wintage cardiology | Tagged coronary angioscopy, intra coronary imaging, ivus, oct, red thrombus, white thrombus, yasumi uchida, Yasunori Ueda, yellow palque | 1 Comment »
Is Transient Ischemic attacks (TIAs) belong to the exclusive domain of cerebral circulation ? Can it occur in the coroanry arteries ? If so what situations ?
This is a presentation in one of the cardiological society of India annual scientific sessions . A pdf download is provided
Posted in Cardiology -unresolved questions, cerebral circualtion stroke, Infrequently asked questions in cardiology (iFAQs), My presentations | Tagged tia equivalents in heart, tia of heart, transient ischemic attacks of heart | Leave a Comment »
Primary PCI is presumed to be the ultimate , undisputed reperfusion strategy in STEMI . Still , time and again one study or other strips down this “Numero Uno” status of pPCI . If it is really supreme , such awkward situation shouldn’t arise too often . More importantly , the major reason for dubious real world record of pPCI goes beyond the time and logistic factors (which is considered the only issue for pPCI by most interventionist ! ) There is something more to it that is invisible ! (Is it the no reflow ?)
The nearly flawless study from Belgium ( STREAM Just released in ACC 2013/Sanfransisco ) , pre-hopsital or early fibrinolysis has proven to be superior in the prevention major end points at 30 days .
- Death
- Re-infarction
- CHF
The major surprise was pre-hospital fibrinolysis showed less incidence of cardiogenic shock . ( pPCI
group had more of this ( 4.4 VS 5.9 % in STREAM )
Now . . . shall I make a provocative statement ?
while pPCI may be treatment of choice for cardiogenic shock . . . but it may also confer a risk of cardiogenic shock in otherwise low risk MI !
Caution and conclusion
STREAM population applies strictly to 1 to 3 hour time window . It does not apply to either before or after that ! Simply put,we do not have guts to compare fibrinolysis and pPCI in patients who arrive within one hour into a facility where 24 hour cath lab facility is available . We call it unethical to do a study like that ! I personally feel it is really unethical if we do not do a study in this time frame . The reasoning is simple and very personal .In a large Government hospital where we do not have primary PCI program our net mortality for STEMI never exceeded 7-8 % over a period of 10 years , Which is almost at par with global data on pPCI. (Our door to needle time is an unbelivebale 8-12 minutes ! that too only streptokinase !)
Adding Further controversy
pPCI is indeed a superior reperfusion strategy . No one can dispute that .But its superiority is not realised in every patient who gets it. The benefits are accrued if and only if it is used most judiciously . In Low risk , small regional , branch vessel STEMI , pPCI has never been shown superior . It is well recognised , upto 15 % of STEMI is likely to spontaneously abort or experience very good spontaneous recannalisation . By rushing these patients very early into cath lab pPCI meddles with the natural anti fibrinolytic mechanisms . It is this population who invite all the procedural hazards. .
Is this the reason STREAM had more cardiogenic shocks in pPCI limb ?
I think STREAM has strengthened the case in favor of fibrinolysis in this ever ending debate .
I would seriously believe pPCI is hanging it’s superiority over fibrinolysis with a wafer thin mortality advantage . pPCI may not be recommended in a routine fashion to all STEMI population even if they arrive within 6 hours and able to perform the plasty fast . Science is . . . after all . . . continuing confrontations with our assumptions !
Counter point
STREAM is not an exclusive study comparing fibrinolysis and PCI . It is a study comparing Pharmaco Invasive approach vs pure invasive approach . 80 % of patients in the fibrinolytic limb ultimately received PCI and stenting . It simply doesnot make sense to conclude fibrinolysis is superior to PCI . Most of the beneficial effects on 30 day outcome may reflect the timely PCI in the lytic group.
//
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Primary PCI, STEMI-Primary PCI | Tagged Pre hospital fibrinolysis, primary pci, STREAM study | Leave a Comment »
Answer :
In cardiogenic shock it is A . In all others it is probably C.
While D may be considered as an essential target criteria for completing the rescue PCI
Read also
Why-we-often-follow-a-reckless-time-window-for-rescue-angioplasty ?
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged rescue angioplasty, rescue pci, time window for rescue angioplasty, waht is the time window for rescue angioplasty | Leave a Comment »
VPDs are such a common cardiac arrhythmia . We also know most are benign .Still modern science demands to rule out structural heart disease in any patient with multiple VPDs.
When ventricles get irritated it reacts with VPDs . ( The irritants can be anatomical , physiological or primary electrical)
Echo can detect only anatomical irritants .We are recognising more such focus for VPDs . Hence idiopathic VPDs may simply reflect our ignorance ! A focused echocardiogram is required .
The following conditions are often observed in patients with recurrent VPDs
- Posterior Mitral annular calcification (Especially in women ) –Annular VPDs
- Aortic valve degeneration /Bicuspid aortic valve with calcification – Cuspal VPDs
- Mitral valve prolapse in young -Stretch induced Pap muscle VPDs
- Minimal pericardial effusions with adherent epicarditis
- LV false tendons-Stretch VPDs
- RVOT lipid focus -Subclinical ARVD
- LVH and Hypertension –Fibrotic VPDs
- Asymmetric septal hypertrophy
- Scars in MI/ DCMs
- infiltrations in RCMs (Any Interstitial heart disease )
(Conditions 7 and 8 are common disorders myocardium just included to complete the list )
**Please note ,above mentioned entites are anatomical irritants .There is a whole lot of physiological irritants
that can induce VPDs . ( Hypoxia, Excess catecholamines , K + fluxes , acidotic milieu etc ) .
*** Another group is primary electrical diseases inherited channel disease can induce VPDs
Also read
A crash course on ventricular ectopics
Posted in Cardiology - Electrophysiology -Pacemaker, Cardiology-Arrhythmias, echocardiography, Infrequently asked questions in cardiology (iFAQs), valvular heart disease | Tagged premature ventricular beats, structural heart disease and vpds, ventricular ectopic beats, vpc, vpds | 1 Comment »
Answer
The tie is between “B” and “D ”
We know in hypertensive hearts LV primarily fails in diastole . Lungs get congested due to raised LVEDP .Here is a catch . . . if diastole is terribly dysfunctional how can be systole be near normal ? (After all . . . systole is not a distant cousin of diastole !)
How is that high blood pressure maintained in spite of LV failure* ?
Is it due to well-preserved EF and cardiac Index ? or Is it due to extreme levels of peripheral sympathetic activity mediated by catecholamine surge triggered by LVF.
We have attempted to measure LVEF in patients with flash pulmonary edema and acute severe hypertension .It was a real messy echocardiography . We could not conclude much but one thing is clear in acute hypertensive LVF the LV was vigorously contracting in , probably making the option D more correct .
* The other way of reasoning is . . . it is because of high blood pressure the LVF has occurred . LV contractility has no contribution in maintaining the high BP ( Not in line with the age old concept of LV contractility a major determinant of systolic blood pressure !)
(Having said that . . . we also see patients with severe LV dysfunction with severely stunned , ventricles in association with hypertension and LVF . In fact many of the reversible DCMs are due to sudden surge in blood pressure )
Other mechansims of LVF and lung congestion is
- Extreme tachycardia and shortening of diastole
- Mitral regurgitation
- Assocaited CAD unmasked by sudden raaise in heart rate .
Postamble
If this article has confused you a little , It has achieved one of it’s objective . ! I expect more from young cardiology fellows to address the issue !
Reference
This NEJM article authored by Sanjay Gandhi has almost answered the hemodynamics of acute LVF and HT .
Posted in cardiology -Therapeutics, Cardiology hypertension, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged after load -preload mismatch, afterload mismatch, lvedp and ef in lvf, mechansim of lvf in hypertension, waht happens to ejection fraction in hypertensive lvf ? | Leave a Comment »
Can VF be a non sustained arrhythmia ? This question was raised and a single case report was presented
in the annual scientific sessions of Cardiological society of India Meet in year 2008 in Chennai.
I am just reposting it from my archives .
Posted in cardaic physiology, cardiac physiology, Cardiology - Electrophysiology -Pacemaker, Cardiology -unresolved questions, My presentations | Tagged mechansim of ventricular fibrillation, non sustained ventricular fibrillation | Leave a Comment »





















