Whitney Houston Autopsy Reveals Heart Disease

The death of Whitney Houston in some ways represents a medical "perfect storm" - heart disease and a plethora of drugs that can accelerate or aggravate that condition, cardiovascular specialists told MedPage Today.

"A lot of people were surprised that Whitney Houston - according to the coroner's report - had cardiovascular disease, but that was not surprising to me, because we knew she had a least one major risk factor for heart disease, cigarette smoking," said John Gordon Harold, MD, the president-elect of the American College of Cardiology.

Harold, clinical professor of medicine at Cedars-Sinai Heart Institute, Los Angeles, and other cardiologists contacted by MedPage Today said there were several scenarios that could explain how Houston drowned in her hotel bathtub February 11.

- The 'hot tub syndrome' - sedative drugs found in Houston's system might have caused her to fall unconscious and slide under the water. "We see this often in people who have been partying and have sedatives on board," Harold said.

- Cocaine also reported in her body could have caused vasospasm or arrhythmia that caused her to lose consciousness and drown.

- With some coronary arteries substantially blocked, a drug-induced spasm could have closed a diseased artery enough to occlude blood flow, causing a heart attack that caused her to drown.

Whatever the triggering event, the fact that Houston was alone and in a bathtub when she suffered a critical event, prevented timely resuscitation and emergency assistance, and turned the incident into a fatality.

Cocaine and the heart

Acute myocardial infarction (AMI) is the most commonly reported cardiac consequence of cocaine misuse, but significant arrhythmias are also reported. More than 100 case reports of cocaine-induced AMI have been published since the early 1980s.

There are a number of proposed mechanisms of cocaine-induced myocardial infarction. Firstly, in-vitro studies have shown that cocaine activates platelets, increases platelet aggregation and potentiates platelet thromboxane production.

Secondly, the sympathomimetic effects of cocaine induce an increase in heart rate and blood pressure, leading to a resultant increase in oxygen demand by the heart. Cocaine could lead to myocardial ischaemia and subsequent infarction, particularly in the presence of underlying coronary artery disease.

Thirdly, coronary artery vasospasm has been suggested as another mechanism for cocaine-induced AMI. The mechanism by which cocaine may induce vasospasm is not understood. There are two schools of thought suggesting a wide role for cocaine as a general vasoconstrictor, and another suggesting a more specific role for cocaine on the vascular smooth muscle leading to vasoconstriction. Of particular note is a study showing the possible role of endothelin-1, the most potent endogenous, endothelium-derived vasoconstrictor factor. That study showed a significantly increased concentration of endothelin-1 in actively intoxicated and chronic users of cocaine over healthy control subjects. However, it was difficult to determine whether this increase alone was sufficient to induce coronary vasospasm. The study went on to hypothesise that, because endothelin-1 increases the calcium sensitivity of arteries, it may sensitise the vasculature to other vasoconstrictor stimuli and prolong coronary vasoconstriction or vasospasm, causing acute myocardial infarction even in people without coronary stenosis.