Dr Malik @ British Cardiac Society Annual Conference


An excellent summary of modern management was presented on Monday Morning 3rd June 2013


Stage 2 Hypertension

Clinic BP 160/100. 24 HR BP 150/95

Stage 1 HT

Clinic BP 140/90. 24 HR BP 130/95

Now we should use 24 HR BP rather than office BP. It is best predictor of end organ damage and predicts cardiovascular risk. It is the reference standard when the diagnosis is in doubt. A Spanish study suggested 29% of patients on treatment were normal on 24 HR BP! It is also cost effective if the clinic BP is initially noted to be high.


A Spanish study showed that 24 HR BP can unmask uncontrolled HT even if clinic BP is OK in 30% of cases! On treatment control should be assessed with 24 HR BP. This is something that we routinely do.

Treatment target:

Look at overall risk. Those with DM/ stroke/ renal disease guidelines say target less than clinic BP  of 130/80. This is tough to achieve and may not have full evidence especially if symptoms of hypotension occur. Thus less than clinic BP of 140/90 may be adequate. Lower probably is better, as long as you don’t get symptoms.

Extremes of age:

Swedish army recruits showed that BP when young showed that the threshold of risk is 140 systolic and 90 diastolic! Thus even at age 18, the total mortality can be predicted by the BP. It is not clear if treatment will help, but at least  a full risk assessment should be done to see if there is end organ damage. In addition central BP in the aorta may need to be measured and full assessment may be needed with MRI scanning.

Over 80, BP treatment reduced risk of stroke and death. In well people, clinic BP > 160/90 should be assessed and treated. Those with poor health anyway may not benefit and so treatment should not be aggressive.


We must control sodium (Salt), alcohol, fat.


Drug treatment is cost effective. Betablockers are now second class citizens. The other drugs including ACE inhibitors/ARB/ calcium channel blockers and diuretics are better. As well as drugs for BP, statins should be given to lower overall risk of cardiovascular events! This is even with  good BP control.


Hypertrophic Cardiomyopathy (HOCM)

is a muscle disease of the heart.

Major risk factors:

Unexplained syncope- the risk is 2x ESP if it is within last 6 months in witch it is 5x. If more than 5 yrs ago, it is not relevant. If there are 2 or more deaths then this risk factor is apparent in early 20s. This would count as a reason fur a defibrillator! Family history of cardiac death. If under age of 40, or if the relative died with HOCM, is a risk.

LVH- this is on echo and not MRI. A wall of 30mm is very thick, and marks risk especially below age 30. It is rare in the child and if present then is a bad sign.

Non sustained Ventricular tachycardia. This is 3 or more Ectopic beats at a rate > 150. This is present in 20-25%. However it is rare in normal younger patients or on exercise. If present then there is a good reason for worry.

Abnormal response to exercise. Ie can’t increase BP by 25mmHg or a drop of 10mmHg. This is only relevant in younger patients. Under about 40-50. Overall, 40% of HOCM patients have no risk factors and will have a near normal life expectancy. Only 3% of HOCM deaths occur in this group. If two or more risk factors above, them a Defibrillator is warranted. This is 20% of the HOCM population. That is easy.

What about the other 40%? That is challenging and needs specialist advice.  Since 2011, if there is severe LVH, syncope or Family history may be enough for a defibrillator according to US but not UK guidelines. The down side is the risk of inappropriate shocks if a defibrillator has been implanted. Thus LV function, LVOT gradients, apical aneurysms, and genotype are not yet established as major risk factors for risk. Standard electrical testing invasively is not warranted.

Advice on exercise:

Vigorous exercise should be banned in all HOCM cases. Even with no risk factors this is risky. Moderate exercise is good. Ie 80% of age adjusted target heart rate.


This is a tough topic and needs careful management of risk.


Left Ventricular Non-compaction

What is it?

The left ventricle (LV) is dense muscle. Sometimes the LV looks more spongy, like a fish may have. This is not normal for vertebrates. It is unclear it it is a distinct condition. It does have a genetic basic, but it is complex. The genes that can cause other heart muscle disease can cause non-compaction is some families.

Why is it important?

With increased use of echo, the LV can look abnormal. It is a tricky thing to be sure that there is the spongy look of non-compaction. MRI is probably better. Over diagnosis needs to be avoided. There needs to be twice as much spongy tissue as proper compacted tissue.

What can happen?

Heart failure, rhythm disturbances and clot formation can occur. It is important to look at the family history to be sure of what the risks are. Things are worse with more spongy tissues, earlier age, poor LV function, and rhythm problems.


Treat the heart failure. Anticoagulants if poor LV function and in Atrial fibrillation. Defibrillator if syncope, failed sudden death, symptomatic ventricular arrhythmia, poor LV function.


A rare condition, that can be over diagnosed. Specialist help is warranted.

Posted on 03 June 2013
Author: LCC
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