Diastolic
heart failure — no time to relax
(This article was first printed in the November
2004 issue of the Harvard Heart Letter.
For more information or to order, please go
to www.health.harvard.edu/heart.)
Trouble relaxing between beats is a growing
cause of heart failure.
Your heart spends at least half the day relaxing.
This isn’t vacation time, mind you, but
a vital and surprisingly complex part of the
pumping cycle. If you’re lucky, after each
contraction your heart muscle relaxes effortlessly,
springing open to fill with blood. If it doesn’t,
you could have — or be headed toward — a “new” condition
known as diastolic heart failure.
Heart failure means that the heart isn’t
circulating blood efficiently enough to meet
the body’s demands. Until recently, the
term referred mostly to weak, flabby heart muscle
that couldn’t squeeze hard enough to move
sufficient blood around the body (systolic heart
failure). Yet up to half of people with symptoms
of heart failure have thick, muscular hearts
that pump just fine. Their problem is heart muscle
that doesn’t relax properly between beats.
This is called diastolic heart failure.
Although it is sometimes billed as a new condition,
diastolic heart failure has been around as long
as systolic heart failure. We’re just more
aware of it now, thanks to the growing use of
diagnostic tools such as the echocardiogram.
Up to half of the 550,000 Americans who develop
heart failure each year have the diastolic variety.
Why the heart
can’t relax
Open space inside the ventricles can
be restricted by heart muscle that “bulks
up” due to overwork or other causes
or that stiffens and loses it flexibility. |
Active relaxation
A single heartbeat actually has two separate
phases. During systole (SIS-tuh-lee), the heart’s
large lower chambers, the ventricles, contract.
This forces blood out of the heart and through
the arteries. During diastole (die-ASS-tuh-lee),
the ventricles relax and fill with blood in preparation
for the next contraction.
Relaxation isn’t a passive event. It’s
an active process that requires energy, raw materials,
and coordination. And it’s vital to adequate
circulation. If heart muscle can’t fully
relax between beats, then the ventricles can’t
fully open. This curbs the amount of blood they
can collect for the next heartbeat, which means
each contraction pumps less blood than it should.
Such inefficient pumping sends less oxygen and
nutrients to the body. Some people handle this
without experiencing any symptoms. In others,
the higher pressures behind the ventricles cause
fluid to back up in the lungs and legs.
Too thick or too stiff
The heart’s ventricles can have trouble
filling with blood for two main reasons. Overworked
heart muscle can “bulk up,” like
a weightlifter; this reduces the open space inside
the ventricles. Alternatively, the heart muscle
may stiffen and become less flexible.
Bulking and stiffening are sometimes the result
of genetic signals. Most of the time, though,
they have more immediate causes. High blood pressure
is one of the most common causes of diastolic
trouble. Diabetes, cholesterol-clogged arteries,
and narrowed heart valves also contribute to
the problem. Less common causes include conditions
that cause protein, iron, and other substances
to infiltrate heart muscle. Such conditions include
amyloidosis, hemochromatosis, and sarcoidosis.
From the outside, diastolic problems look much
like systolic problems. Like water behind a dam,
blood backs up in the lungs and the rest of the
body. This can lead to
- shortness of breath with mild activity, such
as easy walking
- difficulty breathing, especially when lying
down
- swollen legs and feet.
A simple test called an echocardiogram can tell
the difference between systolic and diastolic
disease. Using sound waves to make moving pictures
of the beating heart, it can detect thickening
of the heart muscle, limited space inside the
ventricles, narrowing of one or more heart valves,
and other telltale signs or causes of diastolic
trouble.
Treating diastolic problems
Diastolic heart failure is a relatively new
entity, so how best to treat it is an open question.
There aren’t yet drugs that reliably help
the heart relax more quickly or more completely.
And few large clinical trials of new and old
drugs included people with diastolic trouble.
Treatment for diastolic heart failure focuses
on relieving symptoms and halting or even reversing
the underlying causes. It usually takes a multi-pronged
approach.
Fluid control. The
more fluid in your body and bloodstream, the
harder your heart must work. Limiting the amount
of salt (sodium) in your diet and watching how
much you drink can ease breathing, reduce swelling,
and lighten your heart’s workload.
Pressure control. The
long-term damage wrought by high blood pressure
can lead to diastolic heart failure or make it
worse. That’s why controlling blood pressure
is one of the best things you can do to avoid
or control this condition.
Rhythm control. Contraction
and relaxation are most effective when the heart’s
chambers work as a team. Atrial fibrillation
(rapid and uncoordinated beats in the upper chambers)
worsens diastolic trouble. Controlling it is
important.
Exercise. The breathlessness
and fatigue brought on by activity often prompt
people with diastolic heart failure to become
less and less active. That may keep symptoms
at bay, but it actually makes the problem worse.
A tailored exercise program can strengthen your
heart, slow your heart rate, and improve the
condition of muscles in your heart and throughout
your body.
Drug therapy. A cornucopia
of medications can help ease symptoms and take
aim at the underlying causes of diastolic disease.
These include
- diuretics (water pills) to get rid of excess
fluid
- beta blockers to slow the heart rate. Fewer
beats per minute means more time for the ventricles
to fill with blood between beats
- calcium-channel blockers and long-acting
nitrates to relax blood vessels, especially
those that feed the heart muscle
- ACE inhibitors or angiotensin-receptor blockers
to reduce blood pressure and reverse some of
the physical changes that lead to thickening
of the heart muscle.
(This article was first printed in the November
2004 issue of the Harvard Heart Letter.
For more information or to order, please go
to www.health.harvard.edu/heart.)
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