Heart of Glass


Heart of Glass

Published on 23rd February 2018

Joseph S R de Saram (JSRDS)

Information Security Architect / Intelligence Analyst / Computer Scientist / Human Rights Activist / COMSEC / SIGINT / TSCM

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but my heart started playing up – this is the nature of the Unstable Angina (“UA”) / Myocardial Infarctions (“MI”)  – they just come at the most inopportune moments.

My current issues are not stress-related as I am in a fantastic mood literally all the time these days. By way of information I managed to get PDS to get my heart medication and I am on that again – the irony is that that now seems to be causing the heart instability.

UA and MI are quite similar, but there are key differences. I can feel the difference as the MI (“NSTEMI”) feels different. In both cases UA/MI is not fixed by Glyceryl Trinitrate (“GTN”) so when I am having an episode not much can be done.

There is a difference between UA and NSTEMI. STEMI is full occlusion. I have had that but it has [miraculously] cleared after a few minutes, leaving only a partial issue.

Coronary Artery Disease - Unstable Angina / Non-STEMI Topic Review

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

 “An acute coronary syndrome occurs when atherosclerotic coronary plaque becomes unstable, leading to a series of events that eventually results in partial or total thrombotic occlusion of a coronary artery. Acute coronary syndromes are categorized into unstable angina, non-ST segment elevation myocardial infarction and ST segment elevation myocardial infarction.”

(the whole article is worthwhile reading).

Only if it is extremely serious and there is essentially an occlusion would cardiac catherization need to be performed as an emergency. The NSTEMI is the one that leads to the elevation of Creatinine Phosphokinase (“CPK”), now referred to as Creatine Kinase (“CK”). Administration of oxygen is the only thing that can assist in minimising brain death but it does not unblock arteries and the heart will still die – the myocytes dying leads to the CK leaking into the blood – the more that die means the greater the measurement of CK at 18hrs.

CK is the only indicator that works properly with me – Troponin I and T do not show anything spectacular, and about 20% of people have this issue . Additionally Troponins can be elevated for plenty of other reasons, so as you said yesterday, simply reviewing Troponins in isolation is not going to work – if I have Acute Coronary Syndrome, with or without ECG abnormalities, and with or without CK elevation, then do we just ignore my distress because Troponins are negative?

You are quite right about Troponins being more akin to tools of marking and measurement – they do not fluctuate quickly and in an A&E they are next to useless. My CK elevates within about 60mins so you need to know that if something happens then people should not get bogged down with lab tests before helping me. I have had multiple NSTEMIs and thankfully in each instance the block has cleared itself.

Additionally Troponin T shows more deviation than Troponin I in my situation so that is something for you to remember 😊.

I want you to look at the first attachment – 

Acute Coronary Syndrome

"We must never forget the lessons of the past in our quest for the future." - JSRDS Baby's First Words Thoughts not words in my case - one of my...

In this pdf the key features are the machine-generated text stating

  • Abnormal R-wave progression, early transition, QRS area > 0 in V2
  • borderline t-wave abnormalities T/QRS ratio < 1/20 or flat T.
  • Borderline ECG

These issues are so obvious that even the machine can detect and flag for follow-up management 😊.

Abnormal R-wave progression

Abnormal R-Wave Progression

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

 “Poor R-wave progression is a common ECG finding that is often inconclusively interpreted as suggestive, but not diagnostic, of anterior myocardial infarction (AMI). Recent studies have shown that poor R-wave progression has the following four distinct major causes: AMI, left ventricular hypertrophy, right ventricular hypertrophy, and a variant of normal with diminished anterior forces.”

Get your health question answered instantly from our pool of 18000+ doctors from over 80 specialties

Brief Answer: it is a non-specific finding. Detailed Answer: Hello, Welcome to Healthcare Magic, I read carefully your query and understand your concern. Abnormal R wave progression is a common is a non-specific finding on the 12 lead ECG that in some cases it could indicate a more serious problem.

Abnormal R wave progression is a common is a non-specific finding on the 12 lead ECG that in some cases it could indicate a more serious problem.

The most common causes are :

Conduction defect like Bundle Branch Block

myocardial infarction of the anterior wall

left ventricular hypertrophy

Anterior Myocardial Infarction

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

 “An anterior wall myocardial infarction — also known as anterior wall MI, or AWMI, or anterior ST segment elevation MI, or anterior STEMI — occurs when anterior myocardial tissue usually supplied by the left anterior descending coronary artery suffers injury due to lack of blood supply. When an AWMI extends to the septal and lateral regions as well, the culprit lesion is usually more proximal in the LAD or even in the left main coronary artery. This large anterior myocardial infarction is termed an extensive anterior.”

Left Anterior Descending Artery - LAD

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

The Widow-Maker Heart Attack

The Widow Maker Heart Attack:

At myheart.net we’ve helped millions of people through our articles and answers. Now our authors are keeping readers up to date with essential information through twitter. Follow Dr Ahmed on Twitter @MustafaAhmedMD

“There are three arteries that run over the surface of the heart and supply it with blood. (See the diagram above.) There is one artery on the right side and two arteries on the left side of the heart. The one on the right is known as the right coronary.  On the left side, which is the main side, we have the left anterior descending (LAD) that runs down the front of the heart and supplies the front and main wall, and then the left circumflex that supplies the side wall. When the main artery down the front of the heart (LAD) is totally blocked or has a critical blockage, right at the beginning of the vessel, it is known as the Widow Maker. (The medical term for this is a proximal LAD lesion). No one knows exactly who came up with the term, but the reason they did is likely that if that artery is blocked right at the beginning of its course, then the whole artery after it goes down. This essentially means that the whole front wall of the heart goes down. As far as heart attacks go, this is a big one, with big consequences if not dealt with appropriately; it’s why we take it so seriously.”

Early Transition

This means that I was having a repolarisation issue – remember from my other e-mail “My Achy Breaky Heart”, that a right coronary artery blockage can cause electrical conductance issues?

Borderline t-wave abnormalities T/QRS ratio < 1/20 or flat T

The T-wave provides an excellent indicator of an ongoing myocardial infarction. It can end up being flat or even inverted.

Borderline T-Wave Abnormalities

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

 “The T wave is the most labile wave in the ECG. T wave changes including low-amplitude T waves and abnormally inverted T waves may be the result of many cardiac and non-cardiac conditions. The normal T wave is usually in the same direction as the QRS except in the right precordial leads (see V2 below). Also, the normal T wave is asymmetric with the first half moving more slowly than the second half. In the normal ECG (see below) the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR. The other leads are variable depending on the direction of the QRS and the age of the patient.”

Differential Diagnosis of T Wave Inversion

Myocardial ischemia

Mitral valve prolapse (“MVP”)

Astonishingly, what ended up saving in my life is that only a week or so earlier (10 May 2013) I had gone to my local GP because I was having heart pains who was very concerned that I had Mitral Valve Prolapse. So after I was feeling sick on 18 May 2013 I decided to take a cab to the hospital just to get it checked out. When I first had the MI it felt like indigestion so I went to McDonalds first 😊. Then I felt really sick an hour later and thought it might not be me being hungry. On the way I had a huge myocardial infarction!!

20130510_000000 JDSSG Mitral Valve Prolapse Referral Dr Lim Jiun Jye referral to Dr Koo Chee Choong Consultant Cardiologist

20130510_000000 JDSSG Mitral Valve Prolapse Referral Dr Lim Jiun Jye referral to Dr Koo Chee Choong Consultant Cardiologist (PDF)

The problem here is that unlike Military Intelligence / Law Enforcement operations, I can’t tell my heart to FARC off 😊

The next two PDFs:-

20130518_193300 JDSSG CPK 257 Troponin T 5.7 Dr Victor Lim Parkway Laboratory Services

20130518_193300 JDSSG CPK 257 Troponin T 5.7 Dr Victor Lim Parkway Laboratory Services

CPK 257H confirms that CK is elevated – in my cardiac enzyme, anything above 120 is an issue, for CK (total) and CK Myocardial Band (“CK-MB”) is normally zero.

20130519_084900 JDSSG CPK 402 Troponin T 6.1 Dr Victor Lim Parkway Laboratory Services

20130519_084900 JDSSG CPK 402 Troponin T 6.1 Dr Victor Lim Parkway Laboratory Services

CPK 402H confirms that CK is now over 400 – that means serious, irreparable damage to my heart.

20130520_022131 JDSSG Normal ECG Dr Victor Lim Consultant Cardiologist

20130520_022131 JDSSG Normal ECG Dr Victor Lim Consultant Cardiologist

Dr Victor wanted me on a treadmill, to form a stress test. I had no problems performing that and the ECG is absolutely normal. Also there were no heart issues on exertion, or angina pectoris. This rules out stable angina by the way.

20130520_083500 JDSSG CPK 301 Troponin T 5.1 Dr Victor Lim Parkway Laboratory Services

20130520_083500 JDSSG CPK 301 Troponin T 5.1 Dr Victor Lim Parkway Laboratory Services

A further CPK test shows 301H which further confirms that myocardial ischaemia. But note how the ECG is normal but the CK is still confirming damage and is at a level of 600% my norm of 50? – this is the unique situation I am talking about, when the ECG does not reflect physical damage to the my heart – so if we considered the ECG in isolation without the CK tests, then the diagnosis would be wrong. This is important Lucille!!!

20130522_000000 JDSSG CPK 402 Peak at 18hrs

20130522_000000 JDSSG CPK 402 Peak at 18hrs

The final spreadsheet is the analysis of the 3 CKs and 3 Troponin Ts.

First and foremost, my own baselines are different to the ‘standards’. For example for my CK-MB is normally zero, so for it to go up peaking at 18hrs is the key, not necessarily the values. CK and CK-MB all elevate in textbook fashion at 18hrs or so, so this is the conclusive test.

CK           257 > 401 > 301

CK-MB  3.1 > 4.2 > 2.3

This means that whilst heart cells are dying, massive sections of other cells in other parts of my body are dying too – that could be the Brain Band (CK-BB) or Skeletal Muscle (CK-MM). So the effect of deprived oxygen means that whilst heart myotes die first, there are cells in other organ systems that are dying too en masse ☹. Therefore my total CK is more relevant in my heart issues, than merely analysing CK-MB in isolation. It is particularly relevant to a situation in which there is a full block, which then clears quickly – the level of total CK is very high, and I have been in a lot of physical pain when these events have happened. I am generally to busy to waste time in hospitals, but these events have been so serious that it has necessitated a visit.

Even TPNT           5.7 > 6.1 > 5.1

I do not think that TPNT peaking and dropping is normal either – in Average Joe’s it is present at a reasonable level even a week afterwards. Mine go up and down like my complex life 😊.

20130000 Am J Cardiol Prognostic Significance of an Elevated Creatine Kinase

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

 specifically states

“In patients with troponin-negative acute coronary syndromes, creatine kinase (CK)-MB elevation predicts a significantly higher risk of death and major acute cardiac events compared with CK-MB negative patients. This risk is accentuated in troponin-negative, CK-MB positive patients who do not demonstrate ST elevation by electrocardiogram.

I have UA, and NSTEMI as the primary type of myocardial infarction, and NSTEMI’s signature finding is literally Non-ST-segment Elevation Myocardial Infarction (hence the name).

My CK-MB has specifically become elevated as confirmed in the lab reports:-       CK-MB  0 > 3.1 > 4.2 > 2.3

And the Troponin levels (if compared to normal people) is a negative test result 😊.

The whitepaper continues:-

“Until recently, the diagnosis of an acute myocardial infarction (AMI) was generally made using the revised World Health Organization criteria of 1979.1 These criteria were based, in part, on creatine kinase (CK)-MB measurements. New data have emerged demonstrating that troponins I and T are more sensitive and specific prognostic indicators in patients with an acute coronary syndrome (ACS). This led to the establishment of a new definition of AMI in 2000 by a joint committee of the European Society of Cardiology and the American College of Cardiology that included either troponin or CK-MB elevation as one of its criteria.2,3 Given the emergence of troponin as a more powerful prognostic indicator, the value of measuring CK-MB in patients with an ACS when troponin measurements are available is now in question. We analyzed the prognostic significance of elevated initial CK-MB in patients with normal initial troponin I levels.

So if Troponins are so sensitive, why do we need CK findings as well? The reason is because some people’s Troponins (such as Joe Pure’s) do not increase in line with the levels set to the levels of positive diagnostic findings. Maybe my CK-MB results are generally lower for the same amount of damage, compared with the norms set by 90% of people?

“The important clinical question is whether recognition of CK-MB elevation in troponin-negative patients with an ACS on presentation has an incremental prognostic value. Our study demonstrates that there is higher

morbidity and mortality in troponin-negative patients with an ACS who have elevated CK-MB enzymes compared with those who are CK-MB negative. The results are concordant with a prior analysis of 25 patients with

elevated CK-MB and negative troponin,6 suggesting that CK-MB elevation may identify a subgroup with higher risk among troponin-negative patients. One might suspect that other clinical parameters, such as electrocardiographic findings, may help risk stratify troponin-negative patients more effectively without the aid of CK-MB status. However, in our analysis, CK-MB status still proved to be independently important in the risk stratification of troponin-negative patients without ST elevation by electrocardiogram, a group that may otherwise be considered a low-risk category.”

And finally, when various clots occur, my resistance to Aspirin is another serious issue.

20140613_000000 JDSLK Left Eye Vision Loss Dr Binara Amarasinghe Consultant Eye Surgeon

20140613_000000 JDSLK Left Eye Vision Loss Dr Binara Amarasinghe Consultant Eye Surgeon

Given the fact that on 13 June 2014 I was already taking daily aspirin at 100mg (my Angiogram was on 21 May 2014), then losing sight in my left eye which necessitated the emergency intervention of an Ophthalmic Surgeon (“transient loss of left eye vision, accompanied by facial weakness and slurring of speech”) is indicative of a clotting issue – maybe a small fragment broke off and then ended up in my left eye / brain etc?

It is worthwhile reading the article, but the symptoms that Dr Binara observed are perfect textbook findings:-

“Clots that form in the eye may cause sudden blindness.”

Central Retinal Artery Occlusion (CRAO)

Eye strokes occur when blockages (occlusions) occur in arteries or veins in the retina, causing vision loss. The severity of vision loss depends on the extent and location of the occlusion(s) and loss of blood flow.

Just as strokes occur in other parts of the body because blood flow is blocked, your eye also may suffer damage when vital structures such as the retina and optic nerve are cut off from nutrients and oxygen flowing through your blood.

Besides having an eye exam to detect signs of an eye occlusion, you’ll also need your family doctor or internal medicine physician to evaluate you for high blood pressure, artery disease or heart problems that may be responsible for the blockage.

If a blockage is found, the type of retinal artery or vein occlusion you have is categorized by its location.

Central retinal artery occlusion usually occurs with sudden, profound, but painless vision loss in one eye. Most people with CRAO can barely count fingers in front of their face or see light from the affected eye.

High blood pressure and carotid artery disease increase your risk of a central retinal artery occlusion or “eye stroke.”

The condition may be preceded by episodes of vision loss known as amaurosis fugax. The cause of CRAO is most commonly a clot or embolus from the neck (carotid) artery or the heart. This clot blocks blood flow to the retina.

CRAO is considered a “stroke” of the eye. Studies show that about two-thirds of patients have underlying high blood pressure and one-fourth of patients will have significant carotid artery disease (plaque with narrowing of the artery lining), cardiac valvular disease or diabetes.

In a recent German study of the underlying risk factors in patients with central retinal artery occlusion, researchers found that previously undiagnosed cardiovascular (CV) risk factors were present in 78 percent of CRAO patients, and 67 percent had CV risk factors in their medical history. The most meaningful unidentified risk factor was narrowing (stenosis) of the carotid artery on the same side of the body as the eye stroke.

Also, 11 of the 84 participants in the study (13 percent) had a stroke either prior to or within one month after diagnosis of CRAO. The study authors concluded a prompt, comprehensive, cardiovascular diagnostic work-up should be considered mandatory for all patients with central retinal artery occlusion.

Your ophthalmologist may diagnose CRAO after an examination of the eye, including a dilated pupil exam. With CRAO the retina will be pale and the vessels narrowed. If you are seen within the first few hours of onset, the retinal signs may not yet be present, and a fluorescein angiogram may be required to confirm the diagnosis. This procedure, which is very safe, entails injection of fluorescein intravenously with retinal photography afterward.

No treatment method has been shown conclusively to benefit CRAO. But if you are seen within 24 hours after acute vision loss begins, many ophthalmologists may attempt to dislodge the embolus through methods such as:

  • Using glaucoma medications to decrease internal eye pressure.
  • Having you inhale 5 percent carbon dioxide gas, then using ocular massage.
  • Performing a minor surgical procedure known as anterior chamber paracentesis, in which numbing drops are used and a small amount of fluid is withdrawn from the front of the eye.

If the embolus can be dislodged, blood flow to the retina may be restored partially. Vision loss is less likely if the occlusion has been present only a very short time. However, studies have shown that the retina suffers irreversible injury after only 90 minutes of blood flow loss (ischemia). Despite all attempts to preserve vision, even when you are seen immediately, most patients suffer severe and permanent visual loss.

[Actually as I realised what it was, a blew into a party balloon that I had lying around, in and out, and then breathed it in – that was the 5% CO2, and then I massaged my own eye – quite a stroke (get it!) of genius]

Some people with CRAO will have temporal arteritis (giant cell arteritis), an inflammatory condition of the arteries, which calls for treatment with systemic steroids to prevent loss of vision in both eyes.

20151024_103834 JDSLK Platelet Clotting Asiri Hospital Laboratory

20151024_103834 JDSLK Platelet Clotting Asiri Hospital Laboratory

The report confirms that “There is no platelet response to AA” – AA is Arachidonic Acid, and the flat blue line on the graph.

Platelet function abnormalities in response to arachidonic acid in the acute phase of myocardial infarction

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

When I am suffering from Acute Coronary Syndrome, especially the acute phase of myocardial infarction, then the underlying platelet aggregation problem just fucks me even more 😊

Profile and prevalence of aspirin resistance in patients with cardiovascular disease

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

Clinical implications of aspirin resistance

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

Aspirin (acetylsalicylic acid) is one of the main therapeutic medications used in the prevention of thromboembolic vascular events. Aspirin exhibits its antiplatelet action by irreversibly inhibiting platelet cyclooxygenase-1 enzyme, thus preventing the production of thromboxane A2 (TXA2). Aspirin resistance, as measured in vitro, is the inability of aspirin to reduce platelet activation and aggregation by failure to suppress the platelet production of TXA2. Laboratory tests of platelet TXA2 production or platelet function dependent on TXA2 can detect aspirin resistance in vitro. The clinical implication of this laboratory definition has not yet been elucidated via prospective trials that have controlled for confounders, such as hypertension, diabetes and dyslipidemia. Large meta-analyses have found low-dose aspirin to be as effective as high-dose aspirin in preventing vascular events, making a dose-dependent improvement in laboratory response clinically irrelevant. Possible causes of aspirin resistance include poor compliance, inadequate dose, drug interactions, genetic polymorphisms of cyclooxygenase-1, increased platelet turnover and upregulation of non-platelet pathways of thromboxane production. However, there is currently no standardized approach to the diagnosis and no proven effective treatment for aspirin resistance. Further research exploring the mechanisms of aspirin resistance is needed in order to better define aspirin resistance, as well as to develop a standardized laboratory test that is specific and reliable, and can correlate with the clinical risk of vascular events. The intent of this paper is to review the literature discussing possible mechanisms, diagnostic testing and clinical trials of aspirin resistance and to discuss its clinical relevance as it pertains to cerebrovascular and cardiovascular disease.

Aspirin resistance

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

Aspirin resistance is the inability of aspirin to reduce platelet production of thromboxane A2 and thereby platelet activation and aggregation. Increasing degrees of aspirin resistance may correlate independently with increasing risk of cardiovascular events. Aspirin resistance can be detected by laboratory tests of platelet thromboxane A2 production or platelet function that depend on platelet thromboxane production. Potential causes of aspirin resistance include inadequate dose, drug interactions, genetic polymorphisms of COX-1 and other genes involved in thromboxane biosynthesis, upregulation of non-platelet sources of thromboxane biosynthesis, and increased platelet turnover. Aspirin resistance can be overcome by treating the cause or causes, and reduced by minimising thromboxane production and activity, and blocking other pathways of platelet activation. Future research is aimed at defining aspirin resistance, developing reliable tests for it, and establishing the risk of associated cardiovascular events. Potential mechanisms of aspirin resistance can then be explored and treatments assessed.

2004 Eur J Vasc Endovasc Surg Aspirin Resistance in Cardiovascular Disease - A Review

20130518_000000 JDSSG Borderline ECG Abnormal R and T-waves Dr Victor Lim Parkway Hospital

A mechanism of resistance has not been firmly

established, but is almost certainly multifactorial.

Issues such as inadequate dose and poor drug

compliance may contribute to the failure of aspirin to

inhibit platelet aggregation. Other factors contributing

to aspirin resistance can be classified into these three

broad groups:

Non-COX1 mediated pathways of platelet activation

Aspirin exerts its antiplatelet effect by blocking the

COX1 enzyme that produces the potent platelet

agonist TXA2 from arachidonic acid. Non-COX1

mediated pathways of platelet activation, such as

platelet activation mediated by serotonin and thrombin,

may contribute to aspirin resistance (Fig. 2).

Persistent TXA2 production despite adequate

COX1 inhibition can occur via an alternative COX2

pathway, found in vascular endothelial cells (VECs)

and smooth muscle cells. COX2, which is strongly

induced in vascular disease25 is able to convert

arachidonic acid to prostaglandin H2 (PGH2) which

can be transported into platelets for the production of

TXA2.29,30 COX1 regeneration in nucleated cells such

as macrophages or VECs can also lead to persistent

TXA2 production.19,31

3.8. Clinical impact of aspirin resistance

It is clear that clinically defined aspirin resistance is a major concern, and there is growing evidence that patients with laboratory evidence of aspirin resistance are at a greater risk of thromboembolic events than aspirin responders.19, 26, 58 To date there has been only one prospective study associating suboptimal platelet response to aspirin to a higher risk of adverse clinical outcomes. In a 2-year follow up of 326 stable cardiovascular patients from 1997 to 1999 on 325 mg daily aspirin, 17 (5.2%) aspirin resistant patients defined by optical aggregometry had an increased risk of death, MI, or CVA compared with patients who were aspirin sensitive 

My entire life has been about being uncommon 😊.




Joseph S R de Saram (JSRDS)

Information Security Architect / Intelligence Analyst / Computer Scientist / Human Rights Activist / COMSEC / SIGINT / TSCM