Question
A cath lab is an “optional accessory” in the management of Acute coronary syndrome (ACS).
True or False ?
Answer
“Without a CCU…you can never, treat any Acute coronary syndrome … while we can treat most ACSs successfully without a cath lab “ (If you still got the answer wrong …sorry, no comments)
Best comment
Accessory is ok , but it is “20% foolish” to state cath-lab is optional, it should be mandatory.
Posted in acute coroanry syndrome, acute coronary syndrome | Tagged acc aha esc guidlines, coronary care unit, pci, ptca, role of cath lab in cardiology |
What will happen if you happen to thrombolyse Wellen syndrome?
Answer:
4 will be answer for most of us , while 2 and 3 is a lesser, but distinct possibility. I have never seen 1 happen .Whatever is the correct answer , response 5 will always be correct.
What is the criteria to diagnose Wellen syndrome ?
The criteria used to diagnose Wellen syndrome include symmetric and deeply inverted T waves or biphasic T waves in leads V2 and V3 in a pain-free state, plus isoelectric or minimally elevated (<1 mm) ST segment. In addition, the criteria require the absence of precordial Q waves, the presence of history of angina, and normal or slightly elevated cardiac serum markers.
Wellens is a glorified subset of ACS. It can be referred to as an ACS in a confused state of evolution. Most often a critical mechanical LAD lesion is noted. Thrombus, by no means is excluded. This is the reason some times lytics work. Spasm of epicardial coronary artery is also part of the problem. Since Wellens patients exhibit dynamic symptoms akin to their T waves (often in an inverse relation), it is natural that cardiologists are also tentative, especially if these patients have hypertension and LVH as well.
1.How to manage Wellen syndrome?
Majority of Wellens end up as NSTEMI, statistics tells us about 20% of them can be STEMI in incognito mode demanding lysis or emergency PCI. Since lysis is harmful in subtotal occlusion, it is safe to take all Wellens to cath lab and decide thereafter.
2.Is Wellens exclusive to LAD ?
No. RCA and LCX Wellens do occur, making this entity’s perceived unique importance less certain
3.How common is thrombosis in the culprit artery of Wellen syndrome ?
It is generally believed it is more of a mechanical plaque lesion. However by no means, we can say thrombosis do not occur. This is the reason lytics sometimes work , though we argue it as apparent contraindication.
4.Is there a benign face of Wellen syndrome ?
Yes, we believe so. If Wellen presents as evolved Non -Q-MI or as evolved NSTEMI, a term most cardiologist will not agree with existence of such a terminology .(Clinically, stabilised unstable angina also falls under this category)
Final message
It is curious truth, even fearsome STEMI can be effectively managed without knowing the coronary anatomy (with thrombolysis) ,while Wellen’s a lesser emergency demands more urgent knowledge of coronary anatomy .
Reference
Posted in Uncategorized |
15 % of body weight is fat. (10kg) Out of which just 250 mg of cholesterol is streaming in blood. We must understand fat, lipid and cholesterol are different entities. LDL is obviously a target against atherosclerosis. While the total body fat seems to do little in determining blood cholesterol levels, what is more scientifically shocking is the slope of curve between blood LDL levels and plaque burden is rarely linear. Mind you, LDL constitutes .000025% of total fat. We have many other targets in dyslipidemia like free cholesterol, harmful fatty acids, remnant cholesterol, TGLs, dysfunctional HDLs
LDL is not innocent
Cone electron microscopic Image : A macrophage after a diet full of LDL molecules
There are innumerable evidence for LDL, being the enemy number one in human atherosclerosis .It don’t know but, it fully deserve the name bad cholesterol.It looks like it may be counting its last few decades, as the whole pharma industry is activated to destroy this physiological molecule that carries some critical functions in our body. In one of the hyper-educated debate, I asked how low we can bring LDL down ? One leading professor of lipidology with a H index possibly crossing his LDL levels, said, we can go as low as possible , even to zero. He argued for possible eradication of this heinous molecule. No surprise, there was a thunderous applause from the industry benches.
How to go about lowering the LDL ?
Statins are the first line drugs. We have found it is not enough, it doesn’t bring down LDL below 70 in many , enhancing the residual risk .Now, we have found a God sent weapon. PCSK has got into our hands after some stunning collaborative research between geneticists, biochemist and pharma guys. Let us use it judiciously . This LDL receptor regulatory chaperone , prevents its recycling so blocking or reducing its function
This cartoon from the Dr. Libby’s article (Ref. 1) image depicts the potential pathways beyond Evolocumab (Repatha) and Alirocumab (Praluent). PCSK can either be blocked after its synthesis or paralyzed before it is synthesized (RNA manipulation therapy SiRNA). There is one hidden face for PCSK trials as exposed by BMJ report of FOURIER methodology that will argue some caution with this new target.
Bembidoic acid is a also can also join the death game of LDL .It just acts two step above the HMG-CoA axis blocking ATP citrate lyase, . BM-Acid is approved by FDA well before the CLEAR trial by Steven E. Nissen et al NEJM 2023 Leqvio ® (Inclisiran) is also approved in 2023. Soon, we will get vaccines that will promote lipid catabolism.
Ok let us be practical : What does the current guidelines say about LDL target?
It depends upon the risk profile and the guidelines you follow. Numbers to remember are 70, 55, 40 mg
One of my suggestion is to try keep both LDL and HDL as narrow as possible. This would mean both LDL &HDL should hover around 55 -60mg in high risk category
Can we allow the proposed free fall of LDL ? (Ref 2)
If we apply the 50% reduction from baseline criteria, if someone develops CAD at 50 mg, it would mean to reduce LDL to 25 mg, right? This is where the problem starts. LDL, apart from being a carrier of hormones, may have a role in the structural stability of every cell membrane. While, the relationship between LDL and atherosclerosis is so intimate, funnily we have heaps of data that show South Asian population with tons & tons of plaque with normal LDL. The lesson we haven’t learned from the Indian paradox is that there are more unknown and invisible culprits in promoting atherosclerosis and CAD.
*In fact, for the future generations, there is more exciting ignorance waiting to be decoded. CAD without standard modifiable risk factor SMURF is the new agenda (nearly 25% of CAD occurs in the absence of SMURF – Ref -3). In this scenario, whipping a single known culprit and playing the LDL number game among the public mind is not welcome.
Final message
The tendency to portray a physiological molecule LDL , as a sole villain for CAD is not correct. Further ,trying to eradicate it, Implies, inadequate understanding of human lipidology.
Post-amble
Reference
Posted in Uncategorized | Tagged cut off value for ldl, esc aha guidlines for lipids, functions of ldl molecule, good and bad cholesterol, how low ldl can go, inclisiron, ldl, lipid metabolism, lipidology, pcsk inhibitors, repatha |
It was 1823, a genesis of a new thought process in medical publication began. The man who started it all, Dr.Thomas Wakley the founder of the most famous medical journal (Ref 1)
One of his peers described him what sort of an Image he had. “Thomas Wakley the editor as we find him—a courageous challenger of the medical establishment who was usually right and whose language, however tasteless it might seem today, was well suited to the rough and tumble of the time in which he wrote and spoke”
Lancet celebrates 200 year anniversary
On this 200th anniversary Lancet , looks back ,introspects and redefine the agenda of medical profession. We need more and more people like Wakley in the current era.
The Lancet editorial team has come out with two clips one podcast and other a brief video for a total of 28 minutes . If you have enough patience to hear to this , you are probably in the right direction to understand what exactly is the purpose being a Doctor.
After going through the history of medicine through the lens of Lancet, and understanding its original motto, one thing is very clear. Science and research are vital for progression medical science . But, the least important enemy to handle for a healthy planet and mankind is not diseases and afflictions as such, but the unkind behaviour of biased power centres, skewed knowledge, and unhealthy & unequal practices of health care invention and delivery.
Final message
Doctors are primarily healers, all right; more importantly, they are guardians of goodness and justice in healthcare. For this, we need to “Wakleyse the medical education“, meaning, keep a watch always on the true aim and action of medical establishment under which you work . I know, this post might sound pessimistic for many of you, … but that’s where optimistic goals are hidden deep .
Reference
Thomas Wakley (1795–1862): a biographical sketch
Posted in Medical ethics, Uncategorized | Tagged lancet, lancet 200nyears, medical education, medical ethics, principles ofpractice of medicine |
Cardiogenic shock (CS)is the most feared event following STEMI. The incidence is up to 5 to 10% with a mortality rate of around 50-60%. Still, we are finding it hard to bring this down below 50 % .There is one less addressed issue in ACS literature. We tend to perceive CS as an exclusive complication of STEMI. The fact is that NSTEMI can also result in CS is less recognized. The incidence is half of that of STEMI, i.e., 2.5-5%.
Mechanism of CS in NSTEMI
One may ask, how can CS occur in NSTEMI with partial occlusion with a non trans-mural MI. ACS pathophysiology is not that simple. Ischemic LV dysfunction (Global stunning) without necrosis is equally sinister. This is what happens in some high risk sub sets of NSTEMI.
How is CS in NSTEMI different ?
1.Global ST depression (AVR.V1 might show little elevation with considerable overlap of left main STEMI vs NSTEMI )
2.Onset of NSTEMI-CS occurs late (48-72 hrs)
3.Severe multivessel disease is more common (It is likely ,presence fold STEMI , is an important factor that is likely to precipitate CS when a new NSTEMI occurs.
4.Echo is likely to show more of a Global hypokinesia rather than specific coronary territory
5.Mechanical complication, though less common in NSTEMI , Ischemic MR especially with LCX- NSTEMI can be problematic and much commoner than we think.
6. A subset of NSTEMI precipitated by acute severe HT and flash pulmonary edema has excellent prognosis if BP is reduced promptly. (This can be simply a equivalent of HT, with no true supply side ischemia with LVF with global ST depression )
Management
*More or less similar to STEMI with aggressive opening of culprit lesions with few differences. (unlike STEMI, CULPRIT SHOCK trial doesn’t apply here )
*May require CABG more often
*Mechanical circulatory support will be needed in many
*Finally, and importantly, there is more likelihood of systemic factors like sepsis, Anemia, or renal or kidney failure contributing to the CS in NSTEMI than STEMI. In fact, we have observed pre-existing HFpEF can be a contributory factor.
Outcome
There are differing data about prognosis of CS in STEMI vs NSTEMI. Early mortality is higher with STEMI; but, late mortality converges. Ironically, in many patients of CS in NSTEMI, the outcome can be worse than STEMI, as there is no single culprit and myocardial salvage does not appear to be a primary issue. (Ref 2)
What does SCAI guideline say about CS in NSTEMI?
Nothing, yes it is true. Are you surprised ? A search for the word NSTEMI in both these document drew a blank. May I kindly request SCAI team to look in this, CS in NSTEMI deserve better recognition in their guidelines at least in their next edition (Ref 3,4)
I am not sure why SCAI classification didn’t address CS in NSTEMI as a separate entity.
Final message
Surprisingly , CS in NSTEMI is not a well researched entity in cardiology literature. Fellows are requested to analyse the GRACE registry once again or create their own institutional experience.
Reference
Posted in acute coronary syndrome, Uncategorized | Tagged acc aha esc guidlines on stemi shock, cardiogenic shock, cardiogenic shock in stemi vs nstemi, cs in stemi vc nstemi, grace registry, how is cardiogenic shock in nstemi different from stemi ?, iglobal lv stunning in nstemi, ischemic lv dysfunction, ischemic mitral regurgitation, shock 1 trial, shock 2 trial, stone heart |
Posted in Uncategorized | Tagged forbidden quotes, medical education, medical ethics, medical quotes, science quotes, venkat quotes, venkatesan sangareddi |
”It looks like, science oftentimes struggles at the hands of scientists“
The weakest link in medical research is framing the right research question. How will you explain the drama of research on myocardial viability studies that have been going on full steam for more than 3 decades,? Which has become junk now.
This truth came out from a secondary analysis of the famous REVIVED-BCIS2 trial. For the busy guys, the conclusion is given in the box below.
JAMA Cardiol. 2023;8(12):1154-1161.
Final message
We realize, in the game of myocardial revascularisation the quantum of dead tissue determines the outcome of revascularization, not the amount of living tissues. This same question was asked & answered more than a decade ago (2009) on this site, of course without that damning evidence.
March 15, 2009 by dr s venkatesan
Many times, we don’t require large-scale RCTs, years of toil, and efforts wasting resources to prove an apparent sense of thinking.
Posted in Uncategorized | Tagged accc aha esc guid;ines on myocardial revascularisation, cabg, cabg patch study, ischemic dcm, myocardail viablity, pet scan for myocardial viablity, REVIVED BCIS2, viablity study myocardial |
Conservative management conveys two tangentially opposite meaning.
For the superior “physicians & Interventional cardiologists” it would mean
For the “Inferior genre of physicians” it will sound like this
Reference
This is a partial repost from a 2008 article . https://drsvenkatesan.com/2008/11/30/what-do-we-mean-by-conservative-management-why-it-is-often-considered-as-an-inferior-form-of-treatment-in-medicine/
Posted in Uncategorized | Tagged accc aha guidlines, ethics in medicine, GDMT, OPTIMAL MEDICAL THERAPY, principles of practice of medicine, WHAT IS CONSERVATIVE MEDICAL MANAGEMENT |
Which point in ECG is taken as reference for End systolic dimension for LV function assessment?
Marking the end diastolic point in ECG is quiet straight forward. Peak of R wave.(or Q)*
But, what about the reference point for end systole.
Answer: If I say the answer is 5, no one is going to agree. Please note, the relationship between the T wave and the peak systolic phase in echocardiography is weak. Is there any relation at all ? Then, how to measure LV function in echocardiography? There is a electro-mechanical delay in every segment and sequence of cardiac contraction and relaxation, with former piping the later (electricity beats).
Surprisingly (illogically as well), we take the point of maximum thickness in M-mode as end-systolic, which, in fact, corresponds to peak mechanical systole. This point has no consistent relationship with any part of the T wave. We must realize, the clinical cardiac cycle is defined based on sounds, i.e. S1 and S2, while the biomechanical cardiac cycle is different. Similarly, echocardiographic systole is not the same as clinical systole. 2D echo eliminates this uncertainty to a large extent. This is one of the reasons , we are advised and encouraged, not to measure LV dimensions in M mode.(A very tough advice to follow though)
Final message
We are not completely clear yet, in the “ECG vs Echo” time correlation of hemodynamic events. The errors may be in only milli-seconds, still, when planning for Interventions like re-synchronisations, and in the follow up of DCM patients this could matter much.
Reference
Posted in Uncategorized | Tagged ase criteria for lv function measurement, ecg gating in ct scan, ecg gating volume correlation, ecg vs echo gating, end diastole in ecg, end systole in eco vs ecg, end systolic point in ecg, lv function measurement, peak r and peak t systole and diastole, t wave relation with diastole |
Learning resources in the web, has made the traditional methods of learning & teaching almost redundant.
American society of Echocardiography (ASE) has produced this 20 page PDF document, which covers the entire field of echocardiography , in an Illustrative format.
Take a print out, of this and stick in your lab (If you have space) for an Immersive experience. Hope, sharing this document here doesn’t violate any copyright issues.
Posted in Uncategorized | Tagged ase-posters, best-echocardiography-book, echo-manual, echocardiography, illustrative-echocardiography |
Dr.S.Venkatesan MD 