The two most common complications after stent plaement are in-stent stenosis and in-stent thrombosis.

Even though they rhyme, they are very different problems.

In-stent stenosis is when endothelial and smooth muscle hyperplasia cause the lumen of the stent to gradually narrow with time. This usually presents clinically as gradual onset of angina or exercise intolerence as the process occurs slowly over time. 

In-stent thrombosis is when a previously patent stent is suddenly occluded by a platelet thrombus, usually as a reaction to the bare metal of the stent coming into contact with coronary blood and activating mechanisms of platelet aggregation. This can present as acute coronary syndrome, myocardial infarction or sudden cardiac death.

The risk of in-stent thrombosis is most acute immediately after stent placement (when there has been no endothelialization over the stent) and decreases with time. The opposite is true for in-stent stenosis which takes time to occur.

The introduction of drug-eluting stents (DES) has dramatically decreased the incidence of in-stent stenosis. HOWEVER, as drug eluting stents are slower to endothelialize, the risk of in-stent thrombosis (without medication) is higher.

Dual antiplatelet therapy (usually aspirin and clopidogrel although prasugrel or ticagrelor can be substituted for clopidogrel) is of paramount importance after placement of any stent to prevent in-stent thrombosis. However, the duration of therapy is much longer for patients with drug-eluting stents. How much longer? In general, patients who get bare metal stents (not drug-eluting) need dual antiplatelet therapy for a month. Patients with drug-eluting stents are placed on dual anti-platelet therapy for one year or longer.

There is some belief supported by clinical studies that the latest generation of drug eluting stents may require a shorter duration of dual anti-platelet therapy but the current guidelines recommend at least one year.

In either case, after the clopidogrel (or prasugrel or ticagrelor) is stopped, aspirin is still continued indefinitely.


There is no question that it is clinically important to know whether your patient's systolic function is normal or significantly reduced. It can give you an insight in the underlying clinical pathology and inform important decisions about medical treatments such as ACE-inhibitors and defibrillators.


The overall significance of the ejection fraction is misconstrued by many and lead to such problematic assertions as:

  • My patient has a normal ejection fraction and so his shortness of breath/edema/etc is not from his heart. WRONG! Over half of CHF admissions in the US occur in patients with a normal ejection fraction so-called HFpEF (Heart Failure preserved Ejection Fraction). There are things other than systolic dysfunction that can cause heart failure, most notably diastolic dysfunction and valve disease. Echocardiographic estimates of left atrial size and pressure and pulmonary pressure as well as physical exam (think neck veins) and lab tests (think BNP) are more helpful in establishing a diagnosis of CHF than an assessment of LVEF.
  • My patient has an abnormal ejection fraction and so his shortness of breath/edema/etc is from his heart. WRONG AGAIN! There are many patients with stable cardiomyopathies who do not have any symptoms (we call them NYHA class I). They may have shortness of breath from asthma, pneumonia, pulmonary embolism, etc, just like anyone else. 
  • My patient had an EF of 45% last month and now has an EF of 35%, something bad must have happened. NOT NECESSARILY. LVEF on echocardiogram is generally estimated visually. The inter and intra-reader varibility can be quite high. In this case, it would be important for an echocardiographer to compare the two sets of images to make sure there really is a difference. In addition, LVEF changes dynamically with preload and afterload so may be slightly different under different loading conditions (particularly severe hypertension).

Yes, we tend to give patients with ejection fractions under a certain number ace-inhbitors and ICD's but that's because the trials that looked at these therapies (SOLVD, SCDHeFT used 35% as a cutoff) used an arbitrary LVEF cutoff. It's a bit convoluted to think that a patient with an EF of 39% needs an ACE-I and ICD but a patient with an EF of 41% doesn't. (True, Medicare won't pay for it unless an EF under 40% is established but that's a different story entirely).

Bottom line, when you look at the results of an echo, note the left ventricular ejection fraction but also note the equally if not more important items such as right ventricular function, LV diastolic function, LVEDP estimate (E:E' by tissue Doppler), pulmonary pressures and IVC enlargement.




Atrial fibrillation is one of the most commonly encountered medical problems, particularly on an internal medicine or cardiology service.

One of the first decisions in managing atrial fibrillation is whether a rate control or rhythm control strategy will be used. <

Rate control – it is accepted that the patient will remain in atrial fibrillation (or will go in and out of atrial fibrillation if they have paroxysmal AF). However, to avoid complications such as palpitations, congestive heart failure and tachycardia­induced cardiomyopathy, medications are given to slow the ventricular response rate. As the patient will continue to be in atrial fibrillation, the rate controlling medication do nothing to alter the atrial rhythm and rate. Instead they act to increase the refractoriness of the AV node which will in turn allow fewer atrial impulses to conduct to the ventricles, thereby decreasing the ventricular response rate. There are three major classes of AV nodal blocking agents (i.e., rate controlling agents):

  1. Non­dihydropyridine calcium channel blockers: Diltiazem(Cardizem) and verapamil are the two major drugs in clinical use in this class
  2. Betablockers
  3. Digoxin

The non­dihydropyridine calcium channel blockers are the most negatively inotropic (i.e., weaken the heart muscle) of the above agents and should be used with caution in patients with reduced ventricular function. Beta blockers also exert a strong negatively chronotropic effect (i.e., slow the heart rate) on the sinus node and may produce unacceptable sinus bradycardia in patients with paroxysmal atrial fibrillation. Beta­blockers are also negatively inotropic. Digoxin has a narrow therapeutic range and has untoward toxic effects, particularly in the presence of hypokalemia. It is a weak positive inotrope. It exerts its effect via the parasympathetic nervous system and may not be effective during times of sympathetic stimulation (e.g., movement, exercise)

Rhythm Control. The purpose of rhythm control is to get the patient out of atrial fibrillation and to prevent recurrences. Unlike rate control therapies which are aimed at the AV node, rhythm control therapies are aimed at the atrium itself. Rhythm controlling agents (also called AAD or antiarrhythmic drugs) fall into two basic classes:

  • sodium channel blocking agents
  • potassium channel blocker

These are specialized medications with significant potential adverse effects and should only be given by a cardiologist. 

A really good distillation of clinical pearls in the management of atrial fibrilltion can be found at: 

Adding my two cents:

In my experience the people who best benefit from a rhythm control strategy are:

  • Patients who are highly symptomatic with AF
  • Patients in whom rate control is very difficult
  • Patients with CHF (particularly forms of diastolic CHF such as HOCM where active atrial filling can be critical)