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]