The first angiogram was performed by Dr. Mason Sones at the Cleveland Clinic in 1958. It was a landmark event because for the first time, the coronary arteries could be visualized in a living patient. That meant that the diagnosis of CAD could now be made before a victim had a heart atack or died of sudden cardiac arrest. Cardiologists and radiologists could actually see that the coronary artery was narrowed or completely obstructed. Naturally it was assumed that if a coronary artery was obstructed then the blood flow to the heart muscle was reduced, the function of the heart muscle was impaired, the patient's activities were severely limited and exertion would cause chest pain. Furthermore, the greater the narrowing, the greater the reduction of blood flow tothe heart muscle and the greater the risk of heart attack. Accordingly, it was only a matter of time before a markedly narrowed vessel became cmpletely obstructed, and the patient had a heart attack and even died.
These were completely normal assumptions -- for 1958. However, as time went on and more and more patients underwent angioograms and the fidnings were correlated with the patient's symptoms, my cardiologist began to realize these assumptions were not all true. For example, one study involved a group of United States Marine runners who were selected for their endurance. These subjects all had normal stress tests and were made to undergo angiograms. One could not conduct this kind of study on civilians because there was no justification for performing such tests. To everyone's surprise, a substantial proportion of the Marines had significant coronary artery disease. In some, the disease was so severe they were made to stop running. Why did they not have symptoms?
Marathon runners are occasionally known to drop dead suddenly. It has always been assumed the stress of running was responsible. However, my cardiologist remembers a study he was doing with these recording techniqiues on a running team. He was trying to correlate cardiac function with the runners' performances. To his surprise, a number of runners had impaired cardiac function. Since this was a research study, my cardiologist was not allowed to say anything. One day, he received a call from the team's physician, who was also a runner, asking what my cardiologist had fund on a particular runner. In checking the recordings, he informed the doctor that by his assessment, the function of the heart was considerably impaired. When my cardiologist asked the doctor why he wanted to know, he replied both he and the individual in question had both run marathons the week before without any problems. Tragically, the runner had been found dead in bed a few days later and the autopsy had showed severe CAD.
Similar studies had been carried out onn apparently healthy subjects with normal EKGs, but who had abnormal stress tests. These individuals were made to undergo angiograms. A surprising number of such "healthy individuals" turned out to have severe CAD in several vessels. Yet most were extremely active, even running and playing tennis without symptoms. How could that be? Indeed, some had complete obstruction of a coronary artery, yet there was no history of heart attack and their EKGs were entirely normal.
There is a lack of correlation between angiogram findings and symptoms. Some patients have had repeat and serial angiograms done. If CAD were the cause of their symptoms, then one would expect that in patients whose symptoms had progressed, their CAD would have also progressed. But most of the time, there was no change in their disease. Conversely, it was anticipated that in patients whose symptoms had not changed, or even improved, that their coronary artery disease would have remained stable or even improved. Surprise, that, also, was not the case. Their CAD was often actually worse. Could it be there were other reasons, beside CAD, that these patients were having chest pain?
The biggest mystery to my cardiologist came from studies in which the patiengt had narrowing in two coronary arteries, one mild and one severe. These were the ones that were usually rushed into the OR because the severely narrowed coronary artery was expected to close off at any minute. Instead, these patients were followed for several years until they had a heart attack and the angiogram was repeated. Everyone had suppposed that the most severely narrowed artery would have been the one that had completely obstructed. Instead, it was found that in most cases it was the coronary artery that was only mildly narrowed that had closed off and caused the heart attack. What was going on?
So enamored were cardiologists and surgeons with the angiogram, and the money such tests brought in, that in spite of these wide gaps in what the angiogram was reported to show, there was almost no attempt to explain these discrepancies. It was frightening, because if yousubdivided groups of patients with CAD into those who had no symptoms, those that had symptoms that had been present for years but were unchanged, those with sympptoms that were getting worse, those who were about to have a heart attack, those who just had a heart attack and those who were about to die, and gave their angiograms to any cardiologist, and asked him to organize the angiograms and place each in its approrpriate group, HE WOULD NOT BE ABLE TO TELL ONE FROM THE OTHER! He couldn't even tell who was having chest pain fom the angiogram!
How then, can a cardiologist decide who needs bypass surgery and who does not, if he can't tell from the angiogram whether the patients' disease is coming or going?
The angiogram fails to provide any information about the multitude of small coronary arteries that supply blood to the heart.
The angiogram fails to provide information about the function of the heart muscle since cardiac muscle can't be imaged by x-ray.
Angiograms are one of the most useless, but profitable tools your cardiologist uses.
These were completely normal assumptions -- for 1958. However, as time went on and more and more patients underwent angioograms and the fidnings were correlated with the patient's symptoms, my cardiologist began to realize these assumptions were not all true. For example, one study involved a group of United States Marine runners who were selected for their endurance. These subjects all had normal stress tests and were made to undergo angiograms. One could not conduct this kind of study on civilians because there was no justification for performing such tests. To everyone's surprise, a substantial proportion of the Marines had significant coronary artery disease. In some, the disease was so severe they were made to stop running. Why did they not have symptoms?
Marathon runners are occasionally known to drop dead suddenly. It has always been assumed the stress of running was responsible. However, my cardiologist remembers a study he was doing with these recording techniqiues on a running team. He was trying to correlate cardiac function with the runners' performances. To his surprise, a number of runners had impaired cardiac function. Since this was a research study, my cardiologist was not allowed to say anything. One day, he received a call from the team's physician, who was also a runner, asking what my cardiologist had fund on a particular runner. In checking the recordings, he informed the doctor that by his assessment, the function of the heart was considerably impaired. When my cardiologist asked the doctor why he wanted to know, he replied both he and the individual in question had both run marathons the week before without any problems. Tragically, the runner had been found dead in bed a few days later and the autopsy had showed severe CAD.
Similar studies had been carried out onn apparently healthy subjects with normal EKGs, but who had abnormal stress tests. These individuals were made to undergo angiograms. A surprising number of such "healthy individuals" turned out to have severe CAD in several vessels. Yet most were extremely active, even running and playing tennis without symptoms. How could that be? Indeed, some had complete obstruction of a coronary artery, yet there was no history of heart attack and their EKGs were entirely normal.
There is a lack of correlation between angiogram findings and symptoms. Some patients have had repeat and serial angiograms done. If CAD were the cause of their symptoms, then one would expect that in patients whose symptoms had progressed, their CAD would have also progressed. But most of the time, there was no change in their disease. Conversely, it was anticipated that in patients whose symptoms had not changed, or even improved, that their coronary artery disease would have remained stable or even improved. Surprise, that, also, was not the case. Their CAD was often actually worse. Could it be there were other reasons, beside CAD, that these patients were having chest pain?
The biggest mystery to my cardiologist came from studies in which the patiengt had narrowing in two coronary arteries, one mild and one severe. These were the ones that were usually rushed into the OR because the severely narrowed coronary artery was expected to close off at any minute. Instead, these patients were followed for several years until they had a heart attack and the angiogram was repeated. Everyone had suppposed that the most severely narrowed artery would have been the one that had completely obstructed. Instead, it was found that in most cases it was the coronary artery that was only mildly narrowed that had closed off and caused the heart attack. What was going on?
So enamored were cardiologists and surgeons with the angiogram, and the money such tests brought in, that in spite of these wide gaps in what the angiogram was reported to show, there was almost no attempt to explain these discrepancies. It was frightening, because if yousubdivided groups of patients with CAD into those who had no symptoms, those that had symptoms that had been present for years but were unchanged, those with sympptoms that were getting worse, those who were about to have a heart attack, those who just had a heart attack and those who were about to die, and gave their angiograms to any cardiologist, and asked him to organize the angiograms and place each in its approrpriate group, HE WOULD NOT BE ABLE TO TELL ONE FROM THE OTHER! He couldn't even tell who was having chest pain fom the angiogram!
How then, can a cardiologist decide who needs bypass surgery and who does not, if he can't tell from the angiogram whether the patients' disease is coming or going?
The angiogram fails to provide any information about the multitude of small coronary arteries that supply blood to the heart.
The angiogram fails to provide information about the function of the heart muscle since cardiac muscle can't be imaged by x-ray.
Angiograms are one of the most useless, but profitable tools your cardiologist uses.
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