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Primary PCI and its silent encounter with “myocardial neutrophilia”

February 1, 2023 by dr s venkatesan

Myocardial infarction, a gross pathological entity renamed now as STEMI for clinical purposes, continues to be the most famous medical emergency that triggers a series of calls, right from 911 to the ER, that eventually ends up in CCU or a 24/7 cath lab. The heart, can’t wait for all these external responses when it is challenged with a vascular accident. The moment ATO occurs, two things happen. The endogenous fibrinolytic led by native tissue PA (Tpa) tries to get rid of the thrombotic plug by all its means. It succeeds in 15%. We call it spontaneous lysis or aborted MI. Many lives are lost in the remaining before they reach the hospital..

Meanwhile, the immune high-command deputes scores of neutrophils to the ground zero Fig 1) to supervise what is happening and try to heal the injury. It is worth, understanding, that activated WBCs, sort of convert myocardial infarction from a vascular event to inflammatory pathology, as the hour progress.

 

Fig 1  Infarcted myocardium Invaded by neutrophils

 

 

What do these neutrophils do?  

It will be our ignorance, if we think, they simply crowd around the myocytes helplessly, that is hit by ischemia. They are sent with a specific purpose to protect and heal the myocardium. Very often it fails in its mission is a different story. These fighting neutrophils send a subtle signal  of their presence with a mild increase in temperature during ACS  ( Patel  Prognostic usefulness of white blood cell count and temperature in acute myocardial infarction  Am J Cardiol. 2005 Mar 1;95(5):614-8. )

Is neutrophil invasion good or bad for the myocardium?

These are pro-inflammatory cells. meant to promote healing and mitigate Injury. Interleukins and Leukotrienes do have a healing power as well. But, what happens, in reality, is, still a mystery. As of now, it is tempting to think, it does more damage than good. Its role changes over time. 

 Acute reperfusion Injury in Primary PCI 

Neutrophils are quiet obedient cells generally, but once activated, their behavior can’t be predicted. It may start attacking the host cells, We know reperfusion injury is real and poorly understood. Delayed reperfusion, is well known to cause myocyte softening and lysis. What we know for sure is, primary PCI, induced accelerated flushing of these angry neutrophils is definitely related to no flow, microvascular plugging, and cardiogenic shock.  (The fact that no-reflow and reperfusion injury is less of a problem in fibrinolysis  demands introspection)

Diagnostic & prognostic value of neutrophilia 

Neutrophilia is such a nonspecific response, faces ridicule for its clinical utility. But, In reality, it can be a worthy parameter, to time the age of the infarct (or even confirm* the ACS ) in otherwise equivocal clinical presentation.(Ref 2) More importantly, it provides prognostic information. One more potential use is Neutrophil count to guide the timing of surgery post-MI (as in VSR) A neutrophil count could help avoid the active phase of inflammation.

*I recall my surgical professor’s emphasis on leukocytosis to confirm acute appendicitis during the first clinical year. 

Final message 

There is no academic by-law, that forbids full-blown interventional cardiologists from having an affair with basic science. Unless the core science is irreversibly bonded to the bedside, we can never reap the true benefits of translational research. Hematological aspects in STEMI is one such underrated discipline. Also, we must encourage every postgraduate student in pathology/biochemistry/physiology to visit the CCUs or sit in the cath lab gallery more frequently. Watching the cardiology stalwarts plowing through the blocked coronary arteries, racing against time, is sure to kindle young minds, for a potential molecular breakthrough in cell survival and healing following myocardial hypoxia.

Reference

1.Ma Y. Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction. Cells. 2021 Jul 2;10(7):1676. doi: 10.3390/cells10071676. 

2. Thomson SP, Gibbons RJ, Smars PA, Suman VJ, Pierre RV, Santrach PJ, Jiang NS. Incremental value of the leukocyte differential and the rapid creatine kinase-MB isoenzyme for the early diagnosis of myocardial infarction. Annals of internal medicine. 1995;122:335–341. [PubMed] [Google Scholar]

3.. Cannon CP, McCabe CH, Wilcox RG, Bentley JH, Braunwald E. Association of white blood cell count with increased mortality in acute myocardial infarction and unstable angina pectoris. OPUS-TIMI 16 Investigators. Am J Cardiol. 2001;87:636–639. A610. [PubMed] [Google Scholar]

4. Bhatt DL, Chew DP, Lincoff AM, Simoons ML, Harrington RA, Ommen SR, Jia G, Topol EJ. Effect of revascularization on mortality associated with an elevated white blood cell count in acute coronary syndromes. Am J Cardiol. 2003;92:136–140. [PubMed] [Google Scholar]

 

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Furore over FOURIER is (un)warranted : Evolocumab is an Innocent molecule !

January 16, 2023 by dr s venkatesan

Welcome back to the big molecular science of PCSK and its antagonist Evolocumab, a monoclonal antibody designed to target and prevent the LDL receptor catabolism inside the lysosomes. Evolocumab was approved by FDA for aggressive lowering of LDL, following a  customary study published in NEJM 2017, that released this double-edged anti-lipid molecule into the human domain with all fanfare.

It aimed to reduce the LDL as low as possible in selected patients with familial LDLemia & and those who don’t tolerate statins.  Now, a study was silently released in BMJ open, at the fag end of 2002, which is causing ripples in the pharma world in the new year.

In fact, this paper can’t be called a study. It looks more like an FIR. It questions the missing death counts, which were not included in the landmark trial, that led to its approval.  It took time for the news to sink into the world lipid community. 

Final message

I am surprised at the reactions to the reanalysis of FOURIER data. Any reasonably experienced cardiologist will agree, getting regulatory approval with manipulated data and analysis is more of a norm and not an exception (Ref 1). In a trillion-dollar pharma industry, do you think hiding deaths is a big crime? Is there a solution to this menace?  Yes, let us hope so, with movements like this one (Doshi P et all, Restoring invisible and abandoned trials: A call for people to publish the findings BMJ 2013; 346 )

 

Counterpoint (Q&A)

Q  

Damn this post. Don’t blame a phenomenally successful scientific breakthrough that intercepts the immune destruction of LDL receptors. Instead of being cynical, try to come up with a scientific analysis of the FOURIER study. Please read this rebuttal from the TIMI group, https://www.tctmd.com/news/study-alleges-mortality-miscount-fourier-trial-timi-group-disagrees

 A 

I agree, let us not blame Evolocumab. It is an innocent and intelligent molecule. Culprits are elsewhere. It is a reserve drug in a highly selected population with refractory LDLemia.The lesson from the FOURIER  to all the clinical trialists is, when credibility is lost every thing is lost, even truths can become a casualty. We have to live with that. 

Reference

Marcia Angell,the former NEJM editor’s  book

 

Posted in lipid metabolism | Tagged , , , , |

Take a break from cardiology : How to debate a complex topic in a forum ?

January 16, 2023 by dr s venkatesan

Pardon ,this video is nothing to do with cardiology. It is from the archives of the United nations library .This can teach some important lessons in art of communication , sharing to all folks, especially medical students. It was recorded in 1959 in Newyork, UN head quarters.Four 17 year old school girls & boys were invited for a debate on a complex topic. Does God exist ? How do you pray ? and what is the purpose of different religions ?

I keep wondering , how these youngsters accumulated so much wisdom and express it in such a polite manner too. Mind you, this was recorded , when learning happened with out any digital aids.The word Internet was unheard off. No ego, no bluntness, no diatirbes that has become a norm in many debates now. I got a punching lesson from this clip, be gentle when taking extreme views in any topic.

I wish, every medical debate in class rooms should happen this way.The key to succesful debate is, to accumulate knowedge, willingness to question the convention, and respecting the oppositie point of view.

The high point of talk show, was, when the Brazilian girl(due respects, she should be nearing 80 years now) tell us casually some things are not meant to be understood in life .I tell the same when some patients ask too many questions about their illness which may not have an answer.

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Which is the Ideal site to ablate VT circuit ?

January 12, 2023 by dr s venkatesan

Management of recurrent ventricular tachycardia has developed a lot in recent times. Anti-arrhythmic drugs(AADs) were a cornerstone for most recurrent and refractory VTs till recently. Surgeries including CABG,  repair of the aneurysm, and subendocardial resection has helped to control many post-MI ischemic VTs. Soon they became obsolete. Realistically, PCIs had little impact on post-MI VT for some unknown reasons. However, with the advent of ICDs and RF, ablation, a new dimension is added to this field. 

ICDs, though an attractive device, don’t prevent a VT but vow to nullify the consequence of VT. This is problematic. ICDs in spite of their ability to prevent SCD effectively, it has little say in preventing non-sudden deaths of in any form of cardiomyopathy. (In fact, there is some evidence ICDs might increase myocardial damage with inappropriate shocks )

Hence, RF ablation can be called as true curative therapy by extinguishing hot spots of VT genesis. Still, we need to understand ablation is technically creating new dead myocardium (in alreadly  damaged myocardium) and hence, can’t avoid a consequence. More importantly, ablation as a modality is technically more demanding. We have accumulated huge experience with the help of electro-anatomic imaging and cutting-edge hardware in the last few decades. Still, we find it difficult to zero in the target area of RF ablation, with all available techniques of mapping (Activation, substrate, entrainment, and pace mapping) The reason is,  VT circuits can be really complex ones. Not only different loops but also it can travel deep into the myocardium (Intramural or epicardial) making a single approach endocardial often futile. Success rates vary between 60 -70% (Some may claim 90 +)

This post wants the young fellows to take on this fundamental issue and learn in-depth about the arrhythmia circuit.(Get Inspired by Dr. Samuvel Asirwatham of Mayo clinic work )

What is the best site to ablate ventricular tachycardia?

  1. Exit point 
  2. Central isthmus
  3. Entrance 
  4. Inner loop
  5. Outer loop
  • Though logic would tell us we can intercept an arrhythmia by ablating anywhere in the circuit. But the issue here is we need to permanently ablate it. not just interrupting. 
  • The best site to ablate is the exit point or entry point. Maybe isthmus. I am not really sure. But, one thing is clear, the outer and inner loops are not important. Further, live tissues are the culprits and not the scars and infarcted zones. 
  • One more possible answer is to try to ablate all (or maximum) points in the circuits.

How to identify entry points and exit points?

Not a simple answer .EPs apply their life experience to do that, assisted by technology. Not everyone who has a Carto -GPS can do that.

One simple answer for the fellows is, in entrainment mapping,  critical sites can be somewhat arbitrarily labeled as exit, central isthmus, or entrance on the basis of the Stimulus-QRS interval relationship to the TCL. Exit sites will show an S-QRS interval < 30% TCL (QRS onset shortly after pacing), central isthmuses will show an S-QRS interval of 30% to 50% TCL (some delay in QRS onset after pacing), and entrance sites will show an S-QRS interval of 50% to 70% TCL 

Ruairidh Martin et all Circulation: Arrhythmia and Electrophysiology. 2018;11:e006569

Final message 

Key to the successful ablation of VT is the accuracy in choosing the target site. Locating the target is meaningless if we can’t reach that site. Reaching the site is again futile unless we are able to deliver adequate burning or icing with sufficient contact.

Meanwhile, AADs can never be ignored in spite of the apparent side effects, for the simple reason they reach the VT circuits without any fuss. The Pharma industry has almost lost its interest in AAD research and the hyper-talented EP guys are squarely responsible for this unintended consequence.

Future directions

RF energy modification and newer catheter designs will help. While cryoablation shows a promising advantage over RF, it is still to prove its sustained efficiency. Meanwhile, other ablation modes are being tried. Transvascular ethanol ablation and stereotactic radio ablation have both shown promise for arrhythmias that fail other ablation strategies.

Some more questions

  • What is the difference between arrhythmia focus of origin and entry point? 
  • Once the VT is set in, what is the relevance of its origin? 

Reference

One of the very good reviews on the topic.

1.Gustavo S. Guandalini, Jackson J. Liang, Francis E. Marchlinski, Ventricular Tachycardia Ablation: Past, Present, and Future Perspectives,
JACC: Clinical Electrophysiology, Volume 5, Issue 12, 2019, 1363-1383,
2;,W.G. Stevenson, H. Khan, P. Sager, et al.  Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction Circulation, 88 (1993), pp. 1647-1670

3.M.E. Josephson, L.N. Horowitz, H.L. Waxman, et al.Sustained ventricular tachycardia: role of the 12-lead electrocardiogram in localizing site of origin Circulation, 64 (1981), pp. 257-272

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An unpalatable medical quote

January 11, 2023 by dr s venkatesan

Posted in Ethics in Medicine, medical quotes | Tagged , , , , , , |

Missing links in IHD : What is the relationship between Ischemia & cardiac arrhythmias ?

January 5, 2023 by dr s venkatesan

The term Ischemic heart disease (IHD) was once very popular, but many abandoned it as it became an academic cliche.  CAD & CAHD are the other terms that are equally popular and prevalent. Stable IHD was in vogue till recently, which was again replaced by “chronic coronary syndrome’ now. Honestly, I feel the original term IHD to be restored however outdated it may look. it encompasses the entire spectrum of clinical cardiac disorders.

Manifestation of Ischemia heart disease 

  1. Angina
  2. Infarction
  3. Cardiac failure
  4. Arrhythmias 
  5. Silent ischemia
  6. Sudden cardiac death

 The purpose of this post is to share some thoughts on the link between Ischemia and cardiac arrhythmia. 

 

 

What is the relation between  Ischemia and cardiac arrhythmia (especially VT)

A.Strong relation

B.Weak relation 

C.No relation 

D. Recurrent ischemia protects against arrhythmia.

The fact that. acute Ischemia triggers primary VT and VF and is the leading cause of electrical death is sufficient to fix the answer without any doubt. But, the  truth is, the link between Ischemia and cardiac arrhythmia is more complex  

If we could agree ischemia is a powerful trigger of ventricular arrhythmia, will every patient with chronic stable angina be at risk of  VT after walking a certain distance?  

So, where does cardiac arrhythmia fall in the Ischemic cascade of events? the fact that chronic ischemia on exertion rarely precipitates an arrhythmia conveys a strong hidden message. 

Coming back to, STEMI where the arrhythmic risk is powerful, still, if the same acute ischemia, presents as UA/NSTEMI, with severe compromise of resting blood flow, it doesn’t trigger a VT usually. This fact should baffle us and question why even acute ischemia carries low arrhythmic risk except when it happens with STEMI.

The potential mechanisms of lack of VT in UA* (No evidence /Class C evidence) 

  • In UA, ischemia is primarily subendocardial, and the neuronal innervation which is more in the epicardial plexus fails to get stimulated. This is in contrast to what happens in STEMI. Here It is transmural ischemia and the sub-epicardial is always involved.
  • In this context, the high prevalence of VT in Prinzmeal angina where there is subepicardial injury is a point to be noted. In young NSTEMI/STEMI crossover entities like Wallens and De-winters, there is a high adrenergic drive, which triggers the VT rather than ischemia per-se.
  • Finally, even in STEMI, only a minority of 15-20 % of myocardium become arrhythmogenic and face fatal complications. What protects the rest of the 75 %? is genetics, epigenetics, or fate.? 

The practical implication of this question

  1. The VT in ischemic cardiomyopathy is related more, to the scar burden, strategically placed islands of dead and live tissues, and the overall severity of LV dysfunction. This makes the Ischemic VT, as a term,  could be a misnomer.  In fact, it is the viable ischemic tissue that is a powerful trigger.
  2. If baseline chronic ischemia is less likely to trigger any VT, revascularisation in chronic CAD (PCI/CABG) is unlikely to give relief from it as well.

Anti-arrhythmic adaptation in chronic Ischemia 

We know about ischemic preconditioning and angina relief. It may apply to arrhythmic preconditions as well. Recurrent ischemia, while we expect to elevate the arrhythmic risk, it is a curious and exciting possibility it might work as an “anti-arrhythmia vaccination” at the molecular level. 

Final message 

So, what is the true relation between ischemia and cardiac arrhythmia?  

It is not as strong as one would believe it to be( Except in the early hours of STEMI and a very small subset of NSTEMI.

Curiously, in certain lucky beings, recurrent baseline ischemia may protect against future arrhythmias.

Reference 

1.A V Ghuran, A J Camm, Ischaemic heart disease presenting as arrhythmias, British Medical Bulletin, Volume 59, Issue 1, October 2001, Pages 193–210, https://doi.org/10.1093/bmb/59.1.193

2.Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 1989:  69 ; 1049 –169

Few more questions worth pondering 

Why do certain VTs struggle to become sustained?

Will discuss this later (Will need to talk about the diameter of the primary Rotor, the Curvature of rotors and source-sink mismatch, etc. )

How often  Ischemia triggers AF?

I haven’t heard of Ischemic SVT, or ischemic AF much. Trying to accumulate more Info on this.

Posted in Cardiology -unresolved questions, Cardiology-Arrhythmias | Tagged |

Reviewing top 10 Interventional papers of 2022 : A good lesson on NSTEMI management

January 3, 2023 by dr s venkatesan

EHJ has listed the top 10 papers in cardiology in the year 2022 in its current issue. 

Kindly go through this when free. While each of the 10 has its own importance, one meta-analysis, I thought was a  real bright spot. Though the message it conveys is nothing new,  it reaffirms an important management principle in ACS. Getting curious? Before going into the paper, a mini pretest

What is your take on these 4 statements on ACS?  True or False

1. STEMI is an emergency, NSTE-ACS* is not an emergency

2. Both are true emergencies.

3. STEMI is definite, yes, but  NSTE-ACS may or may not be (Mind the GRACE score dude !)

4. Even STEMI can be a non-emergency if the patient reports after 24 -48 hours.

(Remind you, NSTEACS = UA+NSTEMI , still often used interchangeably)

Hope we don’t have difficulty in identifying the wrong response. Whatever the answer to this somewhat insulting question to our intellect, forget it. Now, read this paper, which is listed as one of the most read last year. It is about the impact of early invasive strategy in NSTE-ACS.

Kite TA, Kurmani SA, Bountziouka . Timing of invasive strategy in non-ST-elevation acute coronary syndrome: a meta-analysis of randomized controlled trials. Eur Heart J. 2022 Sep 1;43(33):3148-3161.

Conclusion is pasted for the busy guys.

Post-test

  1. What is overall NSTEMI in-hospital mortality? (Everyone knows for STEMI it is around 4-8 %, no one seems to be sure about NSTEMI. I think it can’t be estimated accurately, guess it is 1 -2% )
  2. Is there a primary PCI equivalent situation in NSTEMI?  What are they? (Left main UA with AVR ST elevation comes first on the list)
  3. Based on the urgency to treat how does the ultimate outcome change? (This is what this meta-analysis by Kite et all proved.It is not a new revelation though . Recall the landmark ICTUS study  of 2010 which was largely kept in the dark )

Final message

One lay definition of STEMI is, It is a mass of myocardium under fire. True UA/NSTEMI is, a mass of myocardium, that is threatening to go on fire. When firefighters are able to reach a smoky building before the onset of a fire, no doubt, it looks like a great & awesome response, Isn’t it? Unfortunately, the myocardial landscape is different and NSTEACS is such a heterogenous entity that doesn’t welcome unsolicited aggressive, emergency rescue missions. That’s one of the messages we get (at least I got )from this top-read paper in 2022. 

Reference

1.Emanuele Barbato, Margaret McEntegart, Tommaso Gori, The year in cardiovascular medicine 2022: the top 10 papers in interventional cardiology, European Heart Journal, 2023;, ehac778, https://doi.org/10.1093/eurheartj/ehac778

2.Kite TA, Kurmani SA, Bountziouka V, Cooper NJ, Lock ST, Gale CP, Flather M, Curzen N, Banning AP, McCann GP, Ladwiniec A. Timing of invasive strategy in non-ST-elevation acute coronary syndrome: a meta-analysis of randomized controlled trials. Eur Heart J. 2022 Sep 1;43(33):3148-3161.

3.Damman P, Hirsch A, Windhausen F, et al. 5-Year Clinical Outcomes in the ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes) Trial. J Am Coll Cardiol. 2010 Mar, 55 (9) 858–864.https://doi.org/10.1016/j.jacc.2009.11.026

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Happy new year & memories of 2022 !

January 1, 2023 by dr s venkatesan

Wishing every one of you an Enlightening New year. As we begin a new journey around the sun, yet another time, let us re-dedicate ourself, to use science, for the welfare of our planet & people.

Thank you , for visiting this site and make all its worth.

Just one memory of 2022, lingers ! Retired and left Madras medical college,Chennai after 3 decades, which grew me up as a Cardiologist.

Posted in Uncategorized |

Who can answer this unusual query in mitral stenosis?

December 20, 2022 by dr s venkatesan

I will go with the last response. As for as I understand, we have never quantified Atrial muscle mass properly even in normality. One may be tempted to think there is no purpose to measure it, other than academic reasons. The fact that the incidence of atrial fibrillation in mitral stenosis is not linearly correlating with LA size makes us think, LA mass (Virtual LAH) may have a say in triggering AF.

This post is meant for cardiology fellows. Maybe someone can do a study on this by measuring LA mass pre and post-PTMC, we might get an idea about regression as well. Meanwhile, we are well versed with infiltrative diseases like atria like amyloidosis that can mimic LAH. Currently, we realize fatty infiltration of LA is the common trigger for AF in varied populations.

By the way, readers are welcome to post any specific formula to measure LA mass if they come across .

Reference

A good review of LA anatomy.

Posted in Atrial fibrillation, Mitral stenosis, Uncategorized | Tagged , , , , |

Department of artifact : Normal “wall motion defect” in echocardiography

December 14, 2022 by dr s venkatesan

(This post is about some basics in echocardiography meant for fellows, and echocardiographers. Others can skip please ) 

This is a 27-year-old woman who was referred for routine* cardiac evaluation. What do you see?

What is the diagnosis?

This echo clip is from a woman who is 8 months pregnant. What you are seeing is perfectly physiologically and normal. On lying down there is a mechanical push of the diaphragm altering the LV shape and contraction. In the short axis, the left ventricle is contracting well, but the shape is not spherical in systole implying some desynchrony. Further, the  IVS arena is contracting vigorously, which makes, the other segments appear to be poorly contracting. (Someone could report it as a wall motion defect in antero- lateral segments inviting temporary panic)

It is worthwhile to go through this list of non-ischemic WMA and find the pregnancy at the bottom of the list.

Few more conditions, that can be added to this list

  • Though LBBB is the classical cause for WMA, we have seen even LAFB showing the bumpy motion of IVS and the anterior wall.
  • Some patients with ERS and some patients with Brugada show wall motion defects due to repolarisation heterogeneity. 
  • Regioanl pericarditis
  • Intracardiac scars. Localized fibrosis.
  • Extracardiac tumors 

iFAQ on this topic 

Is this wall motion defect in pregnancy, really an artifact or real? 

They are true artifacts in the sense, the heart is an innocent bystander in this pulsating fight between intra-thoracic vs intrabdominal pressures. A similar situation happens in ascites. 

Any other mechanism other than mechanical push?

WMA due to RV volume overload of pregnancy may also contribute. 

Does this WMA affect cardiac hemodynamics?

Logically it should, but it doesn’t. The normal heart has enormous resilience, it just ignores these subtle pushes from below and keeps working normally. Still, enormous distension of the abdomen especially in twin pregnancies, in small body habitus, can make some women breathless, or orthopenic. I am sure, one of the mechanisms could be this geo-mechanical encroachment.

Final message

Wall motion defects are not synonymous with CAD. There is an important list of non-ischemic conditions that can cause WMA. Cardiology fellows and echo technicians are encouraged to go through the above list one more time. While this knowledge can prevent false alarms, at the same time it is always wise to ask for the ECG before doing echocardiography, and not to miss the omnipotent CAD.

Postamble 

*DIscerned readers might wonder why a routine echo was done in a normal pregnancy. I am surprised to note there is an ongoing fad in this part of the world, to do echocardiographic screening on every pregnant mother to rule out cardiovascular disease. (A luxury even the world’s richest country can’t afford) I am told, this echo is meant to rule out peripartum cardiomyopathy for legal purposes. A spot echo at term can never be going to either predict as an event that is mainly going to happen postpartum. This newfound epidemic of anxiety among obstetricians is unwarranted. 

Reference  

A well-written focused review specifically on this topic 

Yavagal ST, Baliga VB. Non-Ischemic regional wall motion abnormality. J Indian Acad Echocardiogr Cardiovasc Imaging
2019;3:7-11.

 

 

Posted in Cardiology -Hemodynamics, Echocardiography -Normal measurement, Echocardiography-hemodynamics, Teaching points | Tagged , , , , , , |

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