Playing with statistics in medicine…

Finally the therapeutic dilemma came to an end…
There was this young ex-pat patient came to my clinic with new onset atrial fibrillation (irregular heart), as she has hypertension we recommended blood thinning medication (anticoagulation) called warfarin on her. Soon after, another doctor prescribed a new novel anticoagulant A, which costs >100 times more. When she came to my clinic she told me that she has not started the medication, as she was not sure whether it was good or not..
Apparently there was some lack of communication. So I went through a brief counselling till she asked, which one is better? I told her comparing the two, the new one, drug A is of course far better, as has been proven in clinical trials. However, taking warfarin strictly with good INR (a way to check your blood thinning index) is likely going to give you similar protection, with overall higher risk of bleeding – the cost however is the main obstacle.
Now the patient said: I trust your decision, doctor. And I am willing to spend the money….
Knowing she has a very young daughter diagnosed with SLE, I really pity her, and this put me in serious dilemma having to recommend a treatment costing over RM400 (or higher cost for her as foreigner) – and yet there is no sure way to tell her she will benefit more compare to her current treatment – its all about statistic – if the ‘number needed to treat’ is below 30 – then it is something very compelling – but in this case it is far more (167 for efficacy & 67 for serious bleeding)…of course there are other benefits like less interaction with food, drugs, and no need for blood test (INR clinic).
Sighed….in the end I advised her give it a try and see how she tolerates the new medication…today, she came back telling me that the new medication had caused her to have pain, cough and shortness of breath. She happened to suffer from flu as well. Well, not a direct adverse event from the medication, however, to remove the doubt, and due to her reluctance I advised her to revert to warfarin.
The lesson here, decision making in medicine may not be very straight forward especially when cost effectiveness is concerned. Patient counselling is an important part of management, do make the patient aware and understand the benefits and risk of the treatment, as well as potential cost effectiveness.

More on TIMI score

A lot of people have visited my posting on TIMI score, which had been posted quiet a good while ago. Let me update you a bit. There are TIMI score classification for both STEMI and UA/NSTEMI, they are separate of course.

The STEMI TIMI score takes into account many parameters that include ECG changes, presentation time and Killip’s score.

Killip score is a simple but useful risk stratification score of patient’s with MI based on their heart failure status (1 – no failure, 4 – cardiogenic shock).

Both scores are reproduced here (pic linked from cardiachealth.org). From Morrow et al, Antman et al Circ, JAMA 2000

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Is there an ‘easy’ way out to reduce blood pressure?

Anecdote of my personal experience managing my hypertensive patients this week.

At last I was relieved. What I have nearly lost last week, now is back under control!

Last week, I was quite frustated by two cases of severe hypertension patients that came to my clinic. One swas a very elderly lady whom I saw first time, previously treated at another centre. According to her daughter, home BP had been quite labile however lately better controlled around 140mmHg systolic. She was otherwise well with cocominant dyslipidaemia only, no diabetes. Her clinic BP at first measurement was 190/90mmHg. When I rechecked it was still at 180/90. Due to her age and the fact that she was due to undergo cataract surgery, I suggested a few days admission. The daughter declined. She was already on Losartan 100mg daily, so I added 5mg amlodipin to start with, urging the daughter to monitor the BP closely.

Early this week she turned up at the ward for preop admission. Her BP in the ward was still very high at 170-180mmHg. I increased her amlodipin to 5mg BD (sometimes I started this way just to allow patients to cope with the sudden increase in antihypertensive, usual dose of amlodipine is once daily). The next day, her BP was still around 170-190mmHg systolic! I allowed her anyway to undergo the surgery under LA. It went uneventful however the ophthalmologist now handed her case to me for postop BP control.

She is already on amlodipine max dose for at least 48 hours, BP still unchanged. Changing the meds to single pill ARB and CCB combination won’t do much I think, since she was already on both separately, therefore I decided to target a different system. Aldosterone, yes, some of these resistant hypertension may have secondary aldosteronism. I therefore started her on spironolactone 12.5mg once daily. After three doses of this drug, here is the BP monitoring chart…

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Even a minute dose has worked so well in dropping the BP by 20mmHg or more, awesome. This is an indirect evidence of her high sodium retention state (salt retention…secondary to secondary hyperaldosteronism). Well, we have also advised her to curtail salt intake.

Second case was another elderly lady whom I saw before, with severe hypertension. In the past the BP had been under control on atenolol and perindopril. This time she presented again because, according to her, BP check by clinic doctor has been persistently high. At my clinic her BP was 185/100mmHg. Heart rate 88, means not fully betablocked. There was no specific reason, she could be nervous, nothing showed on the ECG. Repeated check found no reduction in her systolic BP, looked dubious, however she also refused admission. I sent her TFT and renal function, and started her on diltiazem slow release (Herbesser R100mg). Last Friday she returned to my clinic, this time her BP had dropped to 140mmHg at home, around 156mmHg at clinic. Not yet at target, but she had moved away from danger zone. Now I changed her perindopril to Coversyl plus adding the diuretic component, to obtain an optimal BP reduction.

In both of these cases we have seen big drop in BP with addition of a single agent. I have maintained my practice of using the first three line of drugs A+C+D in most occasions (A=ACEI/ARB, C=CCB, D=Diuretics), however, there are times when I skip this rule especially in dealing with resistant cases. Whatever it is, the first aim in treating hypertension is to reduce BP to target. Next you have to think of the most appropriate agent, ie one that is likely to confer optimum benefit in term of prognosis. Then I will address comorbidity and risk factors, low threshold in initiating statin especially when there are two or more CVD risks present.

Help, how do I entertain this request to talk about a product I do not really favour…?

I am a doctor, I do not do marketing, I only present evidences…

If someone ask you to give talk to an audience about a product that you do not support, for the purpose of promoting it…what will you do? Hold on, there is some attractive honorarium for it, will you do it?

I was not in that kind of situation, but nearly. Now they had asked me to talk about this product H, that I do use, indeed, but not as my first choice. I have kindly obliged since they approached me in a very persuasive way and I know there is nothing wrong with this product anyway, just that I do not use it enough. Did I do it for money, no way, coz, I gave my agreement even before the rep told me that there is going to be honorarium – true, some company do not really give you anything substantial for speaking for them, I still do accept the invitation. For one, I treat this request as an academic exercise aka my own CME, furthermore it gives me opportunity to meet new people and broaden the horizon of my national appearance.

Here is what I did. First, yes, the product is genuine, endorsed by guidelines. I looked through the literature, some of which were old ie pre-2000, however, on browsing our own clinical practice guidelines, no doubt this product was mentioned as one of the approved treatments, listed at par with other, more established product that I frequently used. Therefore there is no conflict, it’s just that, I did not favour the product, due to my own exposure and previous experience.

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Second, as usual the company gave me the presentation materials. As a practice, I do not adopt the presentation material completely, instead, I will go through each slides and ensure that the content genuine and does not contradict with my own understanding and the established evidence. Then I only picked materials that are fairly neutral in contents, ie not too patronizing of the product, I keep on the generic rather than brand name in almost all the labelling if possible. Any of the material that is doubtful or overbearing of the product will be put aside.

Then I drew my own concept and perspective for the lecture. I outlined what I wanted to present, rather than what the ‘company want me to talk’. Obviously I have to supplement more than half of the content with additional materials obtained from my own research. This is where I like being given the task of giving a lecture, since it gives me the opportunity to explore and hence broaden my understanding of the subject, in a fair and unprejudiced way. Fortunately, this day it is  not very difficult to search relevant references through internet.

On the day when I arrived, the company rep had already set up a computer, and projected the slides of the presentation! I quietly went to the stage, and asked to use my own laptop, telling them that I had prepared my own material, combining with the material they have supplied. They had absolutely no problem with this, so I showed them the entire content of my presentation, to assure them that the presentation ‘does justice to their product’. They appeared to be pleased, in fact at the end of the presentation the company manager praised me for the wealth of contents that I have presented.

Therefore, by carrying out this exercise, I had given a lecture, which was fair, unbiased and highly academic. This was proven, when during the discussion, audience had thrown various questions that were quite general rather than too focused on the product. At the same time, the company were happy since enough justice was given to introduce their product to the intended audience.

You may be interested to know, if there had been occasions when I refused to talk about products? Yes, as far as I can recall twice. One about a product that now is being withdrawn from the market – I was sent for a special training workshop for it, but later declined to take further steps to promoting it. Another was a product, which is good and genuine, but I do not use it so much (very much like this case), but I declined coz the company rep was so pushy, then it was passed on to my junior colleague. There was another invitation for a special expert group of another product, which I had some doubt about its strength of evidence, however, I sat there merely as adviser or to give expert opinion, if it come to the stage of endorsement or promotion, I will have to take a stand depending on the nature of the proposal.

In principle, I found most if not all companies (at least their senior management personnel) will not allow promotion of their products beyond its approved label. Therefore, some of them will insist on going through the presentation material in advanced, not because they want to see how much you are promoting their products, its rather to rule out any off label marketing being presented.

Hearty Sharing about Heart Disease at Batu Enam Mosque Gombak

As a sequel to our successful forum at Alam Damai Cheras last month, where I was the moderator, this time I was invited to speak to the congregation of men and women of this Masjid Lama Batu Enam, Gombak.

The place was a little vague to me, despite the fact that I lived in Gombak about 7 years ago when I first settled in Malaysia. It took me 2 stops at two other mosques that were located nearby. Professor Mokhtar who represented the mosque committee – who happens to be my senior colleague at work had been in communication via FB prior to the event.

There were quite a sizeable crowd of men and women, altogether must be close to 80. The mosque is quite old, it was first opened in 1931. Apparently, when the community  built another newer and bigger mosque, Masjid AsSyakirin, which is located about 1km apart, they decided to leave this mosque intact to continue its function. The unique thing about its mosque, apart from its modest size, is its location which is along the main Gombak road, therefore leaving the attending congregation no space for parking. I was given special previlige to park opposite the mosque entrance, leaving half of the car resting over the heightened kerb.

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Most of the audience were of the older age, there were a few young people including the chairman. They provided a decent Powerpoint projector and a good public address system. I began by flashing a slide denoting someone’s status ‘how to have a good heart’. I assuredly said that people who attend the mosque are on the right way of getting a good heart, since everytime they are leaving their house to the mosque, they would recite the du’a among which so that Allah will give send light to their hearts…

Heart disease as number one killer, is no longer a strange statement, though by producing various data derived from the European and international studies, I boldly stated that the true prevalence of cardiovascular disease (that means all heart diseases plus stroke and peripheral arterial diseases) approaches 40-50% globally. However, most worrying is the increasing incidence among young people, which I spent a while demonstrating with examples, including angiogram picture of a 26 year old patient of mine who presented with MI and severe two vessel disease. Women, albeit young are no exclusion, again I mentioned how a 38 year old woman could present with acute MI and severe three vessels disease requiring coronary artery bypass graft. In addition, I brought another striking example of how I had to perform coronary angiogram on a very young patient of 23 year old, though it was almost normal, the guy has a very strong family history of MI, has diabetes and metabolic syndrome. My point was, coronary heart disease in Malaysia is very aggressive and affect people from a very young age group. The special thing about coronary disease in this young group, they tend to be severe and involve multiple vessels.

Further I went on showing alarming statistics of cardiovascular risk factors, based on the old NHMS figure that more than 60% of Malaysians have at least one cardiac risk factor. Accummulation of risk factors increases one’s risk of getting heart disease. Furthermore certain comorbidity especially diabetes doubles the risk. There are systematic risk predictors that can be used to guide therapy such as Framingham risk calculator and European ‘SCORE’.

Lastly, on prevention. Healthy eating, healthy lifestyle – exercise and weight reduction, plus smoking cessation were emphasised repeatedly throughout the lecture. I also gave brief outline of treatment for coronary disease including risk factors modification, medication and revascularisation. Videos of heart anatomy and function, atherosclerosis and MI, and revascularisations with CABG and PCI were shown.

The question and answer session was lively with audience throwing various questions covering medications, how to deal with symptoms of heart diseases, popular issue such as supplement and types of diets etc.

I would like to thank Prof Mokhtar, the committee of the mosque and all the audience present. I hope I have shared some useful highlight and motivate the people to adopt healthy heart living. Afterall, I feel more satisfied now with the changes in approach of the lecture this time. I do hope to improve this further and would not mind accepting future invitation to speak on the same topic. Well, it’s my small deed, at least I can contribute to the society and educate them on this subject that I posses some expertise on.

When all you see is blood….ugh not another complication!

I am starting the day free and easy. Good start of the weekend when I managed to join the Subuh prayer at the surau, and as usual excused myself as soon as prayer ended, went home and awoke the rest of the household between reciting daily portions of the Quran. Kids have school commitment and football but I didn’t need to send them coz they got their motors. Oh, but my mind is fully occupied and I got so many paperworks to do that I don’t think I am talking about going out – though we have at least 2 functions to attend today, and tomorrow evening is my public lecture at a mosque in Gombak (which I am yet to prepare). Therefore I have a good personal reason not to be at the Perhimpunan Rakyat today – furthermore as I stated in my FB status 2 months ago, I have minor disagreement with the nature of the organisation of this gathering, by any means, I do stand with the people and certainly support the spirit of this gathering. Between the time I am reading my PhD student’s thesis – need to be done by Monday, and I have yet to finalise the slides for my lecture to GPs this Wednesday. Now I must concentrate on all these jobs as my priority and not anything else, ooopss why I am writing my blog now??

Yesterday, at the conclusion of Friday prayers at our mosque at PPUKM, the Imam made an announcement inviting the congregations to join a congregational ‘Solat Hajat’ or ‘Supplication prayer’. Though I rarely join such activity, this time I decided for it, well why not, this would be a form of charity for the day, and there is one special reason, I wanted to make a special prayer for an elderly lady patient of ours (DH) who had sustained a complication from pericardiocentesis (a procedure to evacuate fluid accumulation in the pericardial space of the heart).

Here the (sad) story goes…DH is an 70 plus year old patient who had been diagnosed with left atrial myxoma (a kind of tumour in the heart) and chronic pericardial effusion, previous TB but not sure if the effusion was due to TB. Anyway, she was readmitted two days previously with dyspnoea. I reviewed the echocardiogram which showed features of cardiac tamponade, namely a huge accumulation of fluid giving that ‘swimming heart’ appearance with classic diastolic collapse of right ventricle. Since I was only alerted of the echo finding the day after, I immediately rushed to the ward to find out. A decision was made to transfer her to the coronary care for urgent pericardiocentesis. Patient and family, who initially were opposed to any form of cardiac interventions, had on this occasion agreed to undergo the procedure on the basis that it was urgent. Clinically she was quite stable, no tachycardia but had some features like Kussmaul’s sign and pulsus paradoxus.

Najma our previous Cardiac Medical Officer who is now incharged of the patient had requested my kind permission to perform the procedure, of course fully supervised by me. The first puncture was successful yielding straw colour fluid which clearly meant that the needle was in pericardial space. I helped her to thread the wire, next dilator followed by the pigtail catheter. However subsequent aspiration drew blood stained liquid which colour grew more intense and later evidence of clot. This was suspicious, and I performed bubble test which failed to show bubble appearance neither in the pericardial space nor heart chambers. We have drawn out almost a litre and the pericardial space now diminished. I was a bit wary, anyway concluded that there could have been small blood vessel torn by the wire or introducer, or injury to the pericardial surface in some sort.

The nightmare started when I was called half an hour later, DH collapsed with systolic BP of 50mmHg. Echo was repeated and showed re-accumulation of fluid. Not that fast so something must be wrong. The guys were fast in alerting the cardiac surgeons team. I was baffled, clearly the pigtail was in the pericardium, now still aspirating. In order to clear the confusion I decided to attempt a fresh puncture followed by a new pigtail, however this resulted in the same nature of aspirate, this time, of course more dense haemorrhagic fluid. Long discussion took place with the surgeon who were initially reluctant to proceed due to fear of TB pericarditis. In the end they took the patient to the OT. What was found, was phenomenal. Patient collapsed and went asystole on the table, on opening the pericardium huge amount of clot was found lining up the whole space. Once the clot cleared, the bleeder was found, a distal end of right ventricular branch of Right coronary artery perforation! Thankfully the operation went well and the patient is now recovering.

In this unique scenario of event, I must admit that we had taken all the necessary precautions with no shortcut. Diagnosis was made, supported by clinical assessment, explanation and consent obtained from the patient, family informed, they were made aware of the potential complications, the procedure was performed in the presence of a full compliment of cardiac team, the place was right. Each step of the procedure was taken in a systematic and appropriate manner. How human we are, to give a guarantee that a procedure will not cause complications? In fact, if you believe in Murphy’s law, well God’s law is above all, many times, complications happen when you least expect it. I mean at least in this case, I never expected that the procedure is of a high risk – what is pericardiocentesis if it is not one of routine cardiac procedure that required skill. The fact that the puncture was done by an MO (she was seriously traumatised by this event!) under a full supervision of a consultant – did not in any way make the procedure any riskier or of lesser quality assurance. Every step was done in the best way that we knew, of course it is a ‘blind’ procedure with known risk. I have not seen this kind of complication in my entire life.

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We had once, a junior specialist performed a tap in which the pigtail ended in the right ventricle (I promptly diagnosed this with the bubble injection) – patient survived following successful surgery – this sort of thing is  different in the sense that, something wrong was already detected at the start ie at puncture, in contrast to our situation when the puncture was clearly precise with clear fluid and no blood.

Nevertheless, this incident highlight a few important points. First, diagnosis is important, as much as prompt action. Correct diagnosis will justify the relevant treatment or management. This brings up the point on the necessity of performing the procedure, especially in a reluctant patient such as this case. Second, thorough consultation with patients and family must not be overlooked, explanation of the nature of the procedure and each potential major complications should be clearly expressed. Thirdly invasive procedures with potential for serious complications, must be done with appropriate preparations and techniques. Fourthly teamwork and the presence of adequate personnel helped. When complication happen, most of the time it is, more than likely, better to act in a most comprehensive manner, such as done in this case, when the surgeon was called early and treatment carried out immediately.

God knows what is best, we are only His deputies on this earth who should follow His rules and laws. Let’s pray for the wellbeing of this patient, and not to forget all the caregivers involved, may God keep them in the straight path and give them strength in their hearts and minds to face all these challenges without ever losing hopes.

Finding solace in the midst of complexity and crisis….

From hypotensive crisis to LM stenting…keeping life in balance

I don’t mind leading life full of challenges and crisis. I don’t pray for it, but take it for fact, life is already complicated as it is. It really depends on how you look at it. It is my choice, sometimes there is good in looking at something as crisis, so you can act on it, the positive result may boost your confidence and bring you closer to your goal.

Anyway, life as interventionist is never an easy one. I always try to keep the balance between aggressiveness and safety, between extravagance and moderation, more importantly balancing between harm and benefit in the long term. Unfortunately many of those aspiring interventionists are driven by passion to acquire certain skills or status who go on performing procedures of questionable indications or of debatable benefit. Most often scenario is revascularisations by means of PCI for patients with stable coronary disease.

Nevertheless even when you try to keep a most balanced attitude there would be many occassions when you would be required to act or else be seen as  a loser. Or face a demanding patient who dictates you what to do with his or her coronary lesions…to the extent of telling you which devices and which stents to use (ouch…).

Ok enough of moaning. Lets have a little flashback of the this past 7 days or so in my little intervention world.

When hypotension pays you a visit…

First is how do you face a hypotensive patient on a cathlab table. I had this wonder last week and had to get my mind working fast or else face an embarassing case of a perfectly well patient collapsing during a simple, routine angiogram. The patient is a middle aged man who had a coronary bypass 3 years ago now back with recurrent angina. The operation report indicated that he had a left internal mammary on his LAD and two SVGs, one to RCA-PDA and the other a jump graft to Diagonal and obtuse marginal. I had completed the SVG injection when suddenly noted that patient’s aortic pressure dipping rapidly from 140 to 60mmHg. Patient appeared quite ok though. No significant ECG changes, and I did not think that I had caused any damage to the graft. Since this was an elective case then there isn’t any reason of patient decompensating from an acute closure or the like despite severe native coronary disease.

The access was femoral since it was a graft study. Arterial puncture was straight forward, no haematoma on the site and advancement of catheter did not meet any resistance or anything funny, therefore I would not suspect any peripheral complication like retroperitoneal haematoma or iliac or aortic dissection. What I was left with was the little possibility of anaphylaxis or idiosyncratic reaction from contrast media. I quickly administered hydrocortisone and chlorpheniramine, followed by subcutaneous adrenaline injection. Intravenous plasma fluid was administered and the patient now complained of some funny feeling on his throat and chest. The tongue appeared large and thick. However his breathing not affected and I did not have the previlige of auscultating his lung to detect any ronchi. There were diffuse reddish skin discolouration on his upper trunk.

The BP returned swiftly and the symptoms improved. Now I still had to complete the angiogram by shooting the LIMA. So I changed the contrast media from Iopramide to Omnipaque. However the patient complained of extreme chill and started to shiver, I therefore had to accept suboptimal result by several subselective injection of LIMA to dilineate the distal anastomosis. IV fluid was continued and another injection of steroid repeated later, the patient returned to the ward uneventfully.

I still think its a bid odd to accept anaphylaxis when the patient was ok till that point, rather than having immediate reaction following the first injection of contrast. However the rest of clinical picture very much consistent with anaphylaxis.

Another hypotensive patient…

The above was not an infrequent event and we have a sort of rehearsed protocol to deal with it, dictated by what we think the most likely underlying cause is. However this nightmare of hypotensive patients don’t just happen in the cath lab. More frightening is when it happen in the ward, in the middle of night, managed by your poorly informed MOs (err…most of our MOs are well informed ones).

However, that very same day, while I was doing my daily round in the private ward, Hamat my specialist called me about another patient who was post PCI, having a sudden drop in BP. Reportedly the BP was recorded at 50mmHg SBP on arrival to the ward, from the cath lab! Knowing the patient was post PCI, done by me I was feeling utmost responsibility to salvage him whatever the cost. They told me that there was some ECG changes suspected of acute stent thrombosis, therefore a return to cath lab is being arranged so the freshly implanted stents can be relooked at. Hmm not very convincing I thought. Unless the ECG showed a barn door changes of ST elevation MI, I am not going to buy the idea of stent thrombosis this time. For a patient who just returned from cath lab to develop hypotension, there are lists of things that must be immediately ruled out. Stent thrombosis/reinfarction is just one, another is bleeding of course, especially if femoral route had been employed like in this case. But I am concerned with the third possibility of a tamponade. Well, I was told an echo was done, and the result was negative for pericardial effusion.

However, on arrival the patient was obviously distressed, complaining of central mediastinal chest pain. His peripheries were ice cold. The systolic BP was around 70mmHg, an inotropic support had been started. First I told them to transduce and connect the femoral line to the monitor, what a relieve when the arterial pressure waveform showed systolic reading above 100mmHg. I looked at the ECG – there were some peaked T waves anteriorly, mild diffuse ST changes at the inferior leads. The story, the patient underwent elective PCI of an occluded RCA. The RCA was previously patent proximally with occluded distal/PDA, however on reangio that day, the proximal vessel was already occluded. Therefore I decided to intervene on the proximal-mid section. Wire was successfully threaded distally, presumably to the PDA, I was able to pass small balloon distally with no resistance, however elected not to dilate the distal tree. Proximal to mid RCA was ballooned and subsequently stented uneventfully. Final angiography was fine.

Looking at the ECG there was a distant possibility of a stent thrombosis or in another word unlikely. However I was wary of the chest pain in case a dissection had taken place, not a very likely thing though since there was no ostial stenting performed and angiography did not suggest such harrowing phenomena. Bleeding, retroperitoneal haematoma…hmm I need to work on this fast. Another is bleeding from other source such as sudden GI bleed (with high dose antiplatelets loaded it is a certain possibility) – they had sent the Hb though it was ok I would not take it as final, as the changes in Hb may be seen a little later. Physical examination did not suggest any bleeding cause. Heart sounds quite ok. No pulsus paradoxus etc. Despite the initial echo failed to show any effusion, I decided another echo would do no harm. Surprisingly this time a large effusion was detected with evidence of RV partial collapse.

We arranged an immediate evacuation via pericardiocentesis. Pure blood was extracted, about 200ml or so. Since it was still under 4 hours post procedure, I ordered half dose protamine sulfate. Following the pericardiocentesis, pigtail was left in situ to drain. Echo repeated at two hours did not show any reaccumulation and the Hb remain stable with SBP remaining around 120mmHg, while patient was symptomatically better.

Diagnosis: wire perforation – it typically produces delayed pericardial effusion, since the fluid (blood) accumulation takes place slowly. In fact effusion could develop as late as 4 to 6 hours.

This reminded me of another similar event years ago. Sorry, sometimes you must not trust MO to do everything (my hardworking, trustworthy MOs excluded…). There was this elderly lady who was post PCI with successful implantation of stents to LAD. She was fine on return to ward but about 4 hours later developed hypotension. The MO who called me was quite casual in his presentation, giving impression that ‘its the usual hypotension, I just put up fluid and inotrop it should settle…’. I quickly ordered him to do Echo, he said yes. Alas, I later forgot about the case completely, only to return the next morning noting that patient’s BP was hovering around 80mmHg. Thankfully she was otherwise ok! I was deeply annoyed on finding out that Echo was never done, despite my order…I quickly did one and a large effusion was present. Again, the BP returned spontaneously following pericardiocentesis. Another case of wire perforation.

Other cases of extravasation as result of subintimal passage of wire/devices, or extension of subinitimal haematoma leading to perforation, usually happen more acutely and dramatically, on a small number of cases we fail to revive these patients despite aggressive measures. So do not take things lightly, timing of hypotensive episodes mean a lot.

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And yet…another hypotensive patient!

This was another episode that happened quite a while ago, though simple but let me have it mentioned for the sake of sharing and learning. This was a middle aged man, who had a successful implant of a dual chamber pacing. Returned to ward in a stable form and monitored under routine monitoring. A few hours later I overheard one of the registrars were talking over the phone to an MO in the ward who reported the man has ‘collapsed’ and had low BP. The registrar immediately ordered the ‘routine’ treatment of fluid and inotrope. I shouted, asking what’s the case and was informed that this was the man who we just implanted PPM. Well, I said, get an immediate CXR.

Again, somehow it was a very hectic day that I completely forgotten the case. Apparently CXR was only done sometimes after midnight, a large pneumothorax was diagnosed and a chest drain was performed at 6am in the morning! On knowing the case I was utterly dismayed at the mediocre management of this case. Some people never learned the difference between a routine and urgent or even emergency…

In a patient who is post-PPM implant, becoming SOB or hypotensive, think of pneumothorax. Other cause such as bleeding from the puncture or subclavian/SVC perforation from wire or lead; or RV wall perforation is a rare thing.

Work better when under pressure? Then, take the challenge…

Today is a Thursday. I am yet facing another busy Thursday. By default Thursday is a long cath lab day. However today I had to finish by around 1pm, go home and get ready to drive to the North – Kuala Kangsar where my wife is having a school meeting. Suddenly I recalled that there is a private coronary angiography case coming. And yet, another last minute addition, of a complex left main stenting. I checked the list, there were already 6 cases (including one PCI), not including the two additional cases. How I am going to finish them by midday? No way. As the only in-house Interventional Consultant, I need to be there till the end of the cath lab day. At this 11th. hour I texted David, apologetically begging him to come to my rescue…furthermore, David, I need an experienced colleague presence for that complext LMS case…thankfully David responded favourably, stating that he should turn up in the lab by around midday, which was perfect for me.

As I arrived at cath lab in the morning, the staf informed me that the PCI case did not turn up, another cancellation so we were left with 4, plus the two additional cases of mine. Hmm not a bad start for the day. We started with two angiogram with provisional PCI – both did not proceed. Then I started the private angiogram cases, which turned out to be much longer than expected – well, its a 73 year old man with hypertension and query recent MI. The radial artery was tortuous first of all, which took a while to negotiate, then the brachial/innominate vessels were supertortuous, even to get the catheter down was a challenge, manipulating was out of question. This set me back for almost 40 minutes. Now it’s 1130 time to start the LMS PCI.

This was a man in his 70’s who previously attended a highly reputed centre for his IHD, diagnosed with severe 3 vessels disease and a tight distal LMS, refused surgery. Knowing the centre, I would have expected they offer him PCI option, there was no mention of same, which could mean that the anatomy was complex enough. Yes, it must, with (on report) CTO of the RCA and LCX, and tight proximal LAD in addition of the distal LMS. If this was not bad enough, the man had an impaired LV with EF of 35%, and a stage 2 CKD. He was admitted to the private ward for an urgent cranial surgery for a rapidly enlarging cerebral tumour. Of course the Surgeon and anaesthetic would not proceed with the tight LMS.

I was thinking of options, well there arent much options are there? I could do a dobutamine stress test…if he passed then just keep him on a betablocker and proceed. But knowing the tight LM and LAD, he’s basically left with nothing, DSE itself could be dangerous, apart from the likelihood of yielding result that you already know. Or, let him go as a high risk case, full betablockade, no way, patient would be ultraworried, and the surgeon and anaesthetist would never take the risk, further they would think that I am such a loser for not doing anything….

A last minute decision to perform a LM stenting…? And I just got under 1 hour to do it…

So, I am left with a high risk LM stenting…I thought I will first delineate the anatomy, then possibly intervene with the highest risk lesions alone ie the LM and LAD, thats it. Do I need an AIBP, this has to be kept in mind. So, I fasted the man early morning, ordered an echo – which confirmed the impaired LV function though on new estimate not as bad, EF estimated at 46%, therefore this has taken him away from the higher risk category. Access via femoral, I started with a 6Fr. Coronary angiography showed a tight LMS and proximal LAD which was rather large, occluded proximal LCX and severe ostial RCA lesion with proximal stenosis as well, followed by CTO from mid segment.

Took a deep breath…we loaded the patient with Ticagrelor 180mg, I kept the 6Fr sheath since the LM stenting is not likely going to involve kissing balloon inflation. First I targeted the RCA in order to allow some decent circulation as a backup during the LM stenting. I managed to cross a Pilot 50 wire distally to PDA. However repeated attempt to cross balloons, including a 1mm balloon failed. Finally I settled with POBA of the ostial/prox RCA which now appeared better up to the point of occlusion.

The patient remained stable so I proceeded with the LM stenting. Standard JL catheter, wired with a BMW. IVUS was performed which confirmed tight proximal LAD and distal LM has a circumference of 4.7mm2. No concentric calcium. Means things are favourable for simple balloon followed by stenting now. Since there are sizeable gaps of more than 5mm between the LAD and distal LM lesion, which IVUS proved the area to have less than 50% plaque burden, I have the option of spot stenting the prox LAD and distal left main with two stents with or without overlap. I looked around, David was not around yet, I should keep going in view of time. Next I predilated with 2.5mm balloon, everything went smooth. David just arrived, I felt more relaxed to have a senior and experienced colleague like David around, not that I could not do this alone, its more of getting assurance that I am doing right! David agreed with my strategy.

I choose a 3.5mm x 13 Genous stent for prox LAD lesion, dilated up to 16atm. Then I took a 4.0 x 13mm Genous stent for the distal LM lesion, cross over to LAD but not overlapped with the first stent. Brief inflation over nominal (12atm) performed, there was a momentary chest pain complained though patient remained stable. Angiography and IVUS showed slightly underexpanded stent at the distal LM tight lesion. I therefore went on with a non-compliant balloon postdilation with a 4.0x10mm balloon. Repeat IVUS looked good with areas >9mm2. Final angiography was excellent.

We planned to keep patient on the ticagrelor for at least 15 days, following this he may undergo the surgery. Should an emergency arise, ticagrelor may be witheld and surgery can be undertaken within 3 days.

Praise be to God everything went well. This is a second case of LM stenting pre-op non-cardiac surgey that I had performed successfully with Genous, to allow patient to undergo surgery in a timely manner. According to OCT study, 15 days post implant is enough to give a 70% coverage, which according to renown pathologist Renu Vermani, regarded as minimum coverage required to safely avoid stent thrombosis.

I looked at the time, it was just 15minutes past one. I chatted with David regarding stenting strategy in patients undergoing non-cardiac surgery, and brief update of current DES. Then we spoke about FREEDOM, a latest head to head comparison of PCI with DES vs CABG in Diabetic patients with multivessel diseases. The result, as expected favoured CABG for all cause mortality and reinfarction. There was a trend toward less cardiac death in CABG group though statistically non-significant. The PCI group patients tend to have less stroke, as expected. Another ‘defeat’ for interventionalist? What now after OAT, COURAGE and hence FREEDOM, PCI is getting nowhere better than CABG, or even optimal medical therapy in stable CAD? Interventionalists may still have FAME and FAME 2 to defend themselves, but whichever arguments being put forward, in the overall sense, it is still true that PCI in stable CAD does not confer any prognostic advantage. As for angina relief, it may not be as great, as suggested by COURAGE itself where angina relief were only relevant in the first 3 years.