Hyperacute T wave in Precordial Leads

A 61-year old male presented to our ER with 6 hours left sided chest pain associated with sweating. Pain occurred at midnight at 1am. He was a known case of HTN, type 2-DM and CAG nine months ago showed 70% stenosis in obtuse marginal branch (small vessel) and minor plaque in mid LAD. He was on regular medications including 75mg Aspirin.

On arrival he had minimal chest discomfort. Vitals were within normal limits. ECG taken showed Normal Sinus Rhythm with no ST-T changes. 

However, repeat ECG taken 1 hour later during chest pain showed SR with Hyperacute T waves in anterior leads.

So, is it Anterior STEMI?

Three differentials come when there is hyperacute T wave in precordial leads.

1. Hyperkalemia

2. Early repolarization

3. Anterior wall STEMI

LVH may also lead to tall T waves.

In this ECG, hyperkalemia is ruled out since T wave is not tented, QRS duration is normal. Later on his serum K level was normal.

In early repolarization, R wave amplitude should be tall. But in our case, the R-wave amplitude is very small (V1-V3).

He was taken to the cath-lab and CAG revealed 95% thrombotic occlusion in the mid LAD which was stented with a DES.

His follow-up ECG next day showed SR with minimal ST elevation and T wave inversion in anterior leads. (?Reperfusion T waves). There was no q waves.

He had an uneventful course of hospitalization and discharged 3 days later.

Risk of Being an Interventional Cardiologist

We interventional cardiologists doing CAG and PCI frequently and during these procedures ionizing radiation is used extensively. Radiation in the cath lab is generated using two different modes: fluoroscopy or cine angiography (cine). Actually we are having radiation hazard more frequently than others, despite wearing such a heavy lead apron.

Modern cardiac interventional procedures (CAG and PCI) produce effective doses of 4 to 21 mSv and 9 to 29 mSv respectively and are therefore relatively high (1 mSv is the equivalent of approximately 10 chest x-rays)

Radiation has a cumulative effect and leads to increased risk for many conditions, most notably, cancer. Just recently, an Israeli research team that has been tracking the incidence of head and neck tumors in interventional cardiologists and radiologists has now amassed 36 reports of brain and neck malignancies among physicians working with ionizing radiation in cath lab. The group has identified a total of 36 cases, including 28 interventional cardiologists, two electrophysiologists, and six interventional radiologists. Tumor types included glioblastoma multiforme (50% of cases) astrocytomas (7%), and meningiomas (14%).

We should not forget that Roentgen died from radiation-induced cancer because he did not know the devastating consequences of x-ray exposure. Even in this modern era of technology, radiation safety practices are often ignored. We are so enthusiastic to do cath procedures that we even do not care about ‘cracked lead apron’. Moreover, my cath lab does not have the overhanging lead screen that can prevent radiation exposure to brain. We should have dosimeters that should be read monthly.

Another risk we suffer is the chance of developing orthopedic injury from standing for long periods of time wearing heavy lead aprons. In one study, more than 400 interventionalists were surveyed and 71% of the study population reported some type of orthopedic disease. And it has been reported that the most common cause of early retirement for interventional cardiologists is spinal injury.

At least I am not going to attempt chronic total occlusion (CTO) intervention anymore.

1. Roguin A. Radiation hazards to interventional cardiologists: A report on increased brain tumors among physicians working in the cath lab. SOLACI 2014; April 23, 2014; Buenos Aires, Argentina. (heartwire April 23, 2014)

2. Catheter Cardiovasc Interv. 2004;63:407-11

Spironolactone in Heart Failure with Preserved Ejection Fraction

Nearly 50% of patients with HF have preserved EF (HFpEF). Unfortunately, to date, no treatment has been shown to improve outcomes in this condition.

In Aldo-DHF trial aldosterone blockade failed to improve exercise capacity, symptoms, or quality-of-life measures in a placebo-controlled trial of >400 patients with HFpEF (LVEF >50%, NYHA II-III). However, long term spironolactone treatment in the study led to significant gains in echocardiographic measures of diastolic function.

Recently, the large randomized, double-blind TOPCAT study investigated the prognostic role of spironolactone in patients with HFpEF. In this trial, 3445 patients with symptomatic heart failure and a left ventricular ejection fraction of 45% or more were assigned to receive either spironolactone or placebo. There was no overall benefit of spironolactone regarding the primary outcome composite measure. Neither the time to first hospitalization for any reason nor the time to death from any cause was significantly altered by random assignment to spironolactone. On the other hand spironolactone therapy however raised serum creatinine levels and risk of hyperkalemia.

Cat on the Top--TOPCAT  :)

These disappointing results of Aldo-DHF and TOPCAT uprooted my hope that spironolactone has ‘some but not great’ benefit in HFpEF. And still the cornerstone of treatment of this entity revolves around treatment of underlying cause and symptom guided therapy.

TOPCAT. N Engl J Med 2014; 370:1383-1392

Aldo-DHF trial JAMA 2013; 309:781-791.

Heart Block in Hypertrophic Cardiomyopathy

A 28-year old man, known case of HCM (IVS thickness 20mm, PW thickness 15mm) not on treatment, presented to our ER with syncope 3 episodes. He had third degree AV block in ECG. 

HCM is an autosomal dominant inherited genetic disease characterized by compensatory pathological LV hypertrophy due to sarcomere dysfunction. The incidence of arrhythmias in HCM is well documented. These arrhythmias include AF/Afl, SVT, Sinus node disease, ventricular arrhythmias. Ventricular arrhythmias like VPCs, couplets, and VT are very common (comprising 65% of arrhythmias in Holter monitoring). However, association of AV block in HCM is rarely documented in the literature.

First report of AV block associated with HCM is from Luisada in 1965. They reported AV block in a 10-year old boy who presented with headache during a clinic follow-up. In 1977, Spilkin and colleagues described the case of a 20-year old boy with HCM who subsequently developed AV block.

The cause of AV block in HCM is not clear. Histopathologic reports can describe possible causes. Maron et al—histopathologic examination of the AV nodal tissue was normal, however, continuity of the conduction system was interrupted in the bundle of His. Others reported interstitial fibrosis or myocardial necrosis in the conduction system.

Some believe that if AV block occurs and progresses rapidly to high grade block and then to severe syncope, as in our case, death will be inevitable. It is possible that the sudden appearance of high grade AV block is a more frequent cause of sudden death in adults with HCM than previously suspected. Neuromuscular disease, muscular dystrophy also has the similar presentation (HCM and AV block) but our patient has no symptoms and signs of neuropathy/myopathy. It should be noted that acute and subacute complete heart block are sequelae of alcohol septal ablation for HCM.

This patient was taken to the cath-lab and a temporary pacemaker inserted, now planning for permanent pacemaker insertion.

Ref

Luisada AA. Chic Med Sch Q. 1965;25:169-75
Spilkin S, et al. Circulation. 1977;55:418-22
Maron BJ, et al. Am Heart J 1981;101:857-60

Inferior wall ST-segment elevation in acute anterior wall MI

A 50-year old female, known diabetic under medicine, was referred from a local hospital to our ER. She gave a history of central chest pain associated with sweating and one episode of vomiting. The pain was radiating to her left shoulder. In that hospital she was seen by an orthopedic surgeon who did X-ray left shoulder and found 'nothing'. Then he referred her to a physician who did one ECG which showed some ischemic changes in the anterior leads (see below) and referred her to a cardiologist.

Echo was done and labeled “Normal Echo Study”!!!. She had increasing chest pain and her family members took her to the ER of the same hospital. Another ECG was taken which showed extensive ST elevation in the anterior leads and even in the inferior leads (see below). She was diagnosed as a case of anterior wall MI and referred to our hospital.

On arrival, she had ongoing central chest discomfort. Repeat ECG showed ST elevation in the leads V2-V6 and II, III, aVF. She was taken to the cath lab. Coronary angiography showed near total thrombotic occlusion in the LAD and 95% stenosis in the LCX. Both LAD and LCX were stented with DES and shifted to the CCU.

She is now chest pain free and doing fine.

Inferior ST-segment elevation during anterior wall acute MI due to LAD occlusion is unusual and was rarely investigated. There are some possible conditions where an inferior ST-segment elevation occurs during acute anterior wall MI. 

1. Mass of ischemic anterior wall myocardium is relatively small, resulting in a weaker anterior injury current and less reciprocal inferior ST-segment depression

2. There is concomitant inferior wall transmural ischemia that further shifts the inferior ST segments upward

3. LAD artery extension onto inferior wall of left ventricle ('wrap around LAD')
4. Collateral flow from LAD artery to inferior wall.
(Latter two leads to inferior wall transmural ischemia.)

Ref:

[Am J Cardiol 1992;69:860-5]

PCI without surgical backup: shall we do it?

PCI done without on-site cardiac surgery backup was shown to be as safe as procedures done with on-site backup in several registries. Yes, it is safe and efficacious, but many still raise a question “does any patient prefer to have angioplasty done at a center without surgical backup?"

Then shall we open a cath-lab where there is no surgical backup? In 2011, CMS-TH, Bharatpur established a cath-lab without any surgery backup. Should it be done? I personally agree that there is a desperate need for PCI with no matter surgery backup in remote areas where transit to regional centers is unreliable and awkward. If a patient with acute STEMI collapses in our ER, then can we take a risk to refer him to a surgical backup center that is approximately 6 hours far? So, I believe primary PCI facility should be available in a timely manner irrespective of surgical backup.

What if the patient needed an emergency CABG? I argue, emergency CABG is required in only 0.2% of cases. In one study, the rate of emergency coronary bypass surgery, which was needed by 0.3% of patients treated at centers without surgical backup, and by 0.4% of those treated with on-site backup.

In an effort to evaluate the introduction of PCI care at hospitals without onsite cardiac surgery, the state of California instituted a pilot program comparing PCI results in six pilot and 120 non-pilot facilities. The results of the study were recently released on March 29, 2014—ACC 14.

The study concluded that while pilot without onsite cardiac surgery hospitals performed proportionately more primary PCIs than onsite hospitals and showed a significantly better PCI composite safety endpoint, the pilot without onsite cardiac surgery hospitals had worse composite efficacy endpoints than non-pilot hospitals. Offsite hospitals perform more primary and fewer elective PCIs than Onsite hospitals. Moreover, emergency CABG rates were low in both Offsite and Onsite hospitals reducing the need for Onsite Cardiac Surgery. [PCI-CAMPOS study]

We recently published a paper in JNMA.

Dubey L, et al. Percutaneous coronary intervention without onsite cardiac surgery backup. J Nepal Med Assoc 2013;52(189):267-71

We concluded that despite having no cardiac surgery backup, in-hospital mortality and other complications following PCI were acceptable in our cardiac catheterization laboratory.