Left ventricular hypertrophy is enlargement (hypertrophy) of the muscle tissue that makes up the wall of your heart’s main pumping chamber (left ventricle).
Left ventricular hypertrophy develops in response to some factor, such as high blood pressure, that requires the left ventricle to work harder. As the workload increases, the walls of the chamber grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart.
If you have left ventricular hypertrophy, you’re at increased risk of heart disease, including heart attack, heart failure, irregular heartbeats (arrhythmia) and sudden cardiac arrest.
The incidence of left ventricular hypertrophy (LVH) increases with age and is more common in people who have high blood pressure or other heart problems.
Left ventricular hypertrophy usually develops gradually. You may experience no signs or symptoms, especially during the early stages of development. When signs or symptoms are present, they may include: Continue reading About Left Ventricular Hypertrophy
Celebrex, a popular arthritis drug that blocks pain by inhibiting an enzyme known as COX-2, has been shown in laboratory studies to induce arrhythmia, or irregular beating of the heart, via a novel pathway unrelated to its COX-2 inhibition.
University at Buffalo researchers discovered this unexpected finding while conducting basic research on potassium channels.
They found that low concentrations of the drug, corresponding to a standard prescription, reduced the heart rate and induced pronounced arrhythmia in fruit flies and the heart cells of rats.
The drug inhibited the normal passage of potassium ions into and out of heart cells through pores in the cell membrane known as delayed rectifier potassium channels, the study showed.
Aware that COX-2 inhibitors had been shown to produce cardiovascular side effects, the researchers first tested whether Celebrex would affect the heart in fruit flies, a good animal system for studies on heart in other species, including humans.
The researchers now are examining the underlying molecular mechanisms responsible for the drug’s action and its effect on other ion channels that play a prominent role in setting the rhythm of the heart.