One of the things we are taught early in medical school is that most diagnoses are made by taking a careful history. The exact figure varies depending on which study you quote, but the classic teaching is that around 80% of diagnoses can be reached from the patient’s story alone. I still think that is broadly true. Listening properly matters enormously, both in terms of getting the right information to make a diagnosis, but also as a fundamental part of a good doctor-patient relationship. If I ever see a doctor, or any health professional for that matter, I want to feel heard.
The detail of how symptoms start, what brings them on, what relieves them, how long they last, where they travel, and what else is happening around them often points you very strongly towards the answer. This week however gave me a very neat reminder of the other side of the coin: sometimes the story is compelling, the early tests seem to support it, and yet the more advanced test changes the picture completely.
I was on call on Friday and saw two women, both in later life, who presented with symptoms that sounded very much like heart pain. The first had experienced central chest heaviness some months earlier, particularly in cold weather, with discomfort radiating towards the jaw. That is a very classical description of angina. She had also been caring for her husband and, like so many carers, had rather put her own health to one side. When she later had another episode and was seen by her GP, her ECG was significantly abnormal. To my eye, it looked very much as though she may have had a heart attack some months earlier, with a possibility of further heart pain more recently.
In that situation, the appropriate test was a coronary angiogram. This is where a small tube is passed, usually through the wrist, up to the heart arteries. Dye is injected so that we can see whether there are any narrowed or blocked arteries. These days, we very rarely use invasive angiography purely as a diagnostic test in lower-risk situations, because CT coronary angiography is an excellent non-invasive alternative. But when someone is suspected of having had a heart attack, an invasive angiogram is often the frontline test because if a significant blockage is found, it can potentially be treated with a stent at the same time.
Her angiogram, however, was not what I expected.
There was no significant coronary artery disease.
That was obviously reassuring in one sense. There was no major blocked artery sitting there waiting to cause trouble. But it also meant the story was more complicated. Her abnormal ECG might reflect an inherited heart muscle condition. Alternatively, she may have had a different type of heart attack, such as a small embolic event, or what is sometimes called MINOCA — myocardial infarction with non-obstructive coronary arteries. The next step for her is a cardiac MRI scan, which is very good at looking at the heart muscle itself and helping us distinguish between scarring from a previous heart attack, inflammation, inherited heart muscle disease, and other possibilities.
The second patient had a more sudden onset of central chest discomfort. Her ECG changes looked more recent, and she also had a modest rise in a blood test called troponin. Troponin is released into the blood when heart muscle cells are injured, and it is one of the key tests we use when assessing possible heart attacks. Again, the history sounded convincing. The ECG added weight to the concern. The blood test added more. I was highly suspicious that she had had a heart attack and arranged an angiogram.
Again for the second time that day, her heart arteries looked essentially smooth, with no significant narrowing or blockage.
In her case, given the modest troponin rise, the nature of the symptoms, and the absence of obvious coronary disease or major risk factors, I suspect the more likely diagnosis is myocarditis — inflammation of the heart muscle. This is often viral, often self-limiting, and sometimes needs anti-inflammatory treatment and careful follow-up while things settle. Again, cardiac MRI is extremely useful because it can show patterns of inflammation and injury within the heart muscle that an angiogram simply cannot.
Interestingly, a patient wrote to me this week with a question that links quite neatly to all of this — and also highlights how easy it is to be misled by oversimplified explanations online. They had read about the difference between so-called “hard” and “soft” plaque in the arteries. The article suggested that “hard” plaque is stable and relatively harmless, whereas “soft” plaque is dangerous because it can suddenly break off, travel in the bloodstream, and cause a fatal event — even implying it could travel to the brain. It then went on, somewhat predictably, to promote a garlic-based supplement as a solution.
There are elements of truth in this — but also some important misunderstandings.
In reality, plaque doesn’t typically “break off and travel” in the way that is often described. The more relevant process is that certain types of plaque — often lipid-rich and inflamed — can become unstable and rupture within the artery itself. This triggers clot formation at that exact site, which can suddenly block the artery and cause a heart attack. The concept of “more dangerous” versus “more stable” plaque is real — but the mechanism is quite different from how it is often portrayed.
It is also true that some of these higher-risk plaques are not always obvious on basic tests, which is one of the reasons more advanced imaging — such as CT coronary angiography — can often add useful information.
As for supplements, including garlic-based compounds, the evidence simply isn’t there to support them as a reliable way of stabilising plaque or preventing heart attacks. That doesn’t mean diet isn’t important — it absolutely is — but the idea that a single supplement can meaningfully alter this process is, at best, an oversimplification and, at worst, misleading.
I’ll come back to this in more detail next week, because the difference between so-called “stable” and “unstable” plaque — and what we can realistically do about it — is both fascinating and clinically important.
So, what is the lesson?
It is not that the history was unhelpful. Quite the opposite. In both cases, the history was what correctly identified that these were potentially serious presentations that needed urgent assessment, but the history could not provide the full answer. Nor could the ECG. Nor could the blood test. Even the angiogram, which gave us very important information, did not complete the puzzle. It told us what these patients did not have: they did not have major obstructive coronary artery disease requiring a stent. But it also opened the door to a different set of diagnoses.
That distinction really matters. If someone has a classic heart attack due to a ruptured plaque and blocked artery, the treatment pathway is very different from someone with myocarditis, or an inherited heart muscle condition, or MINOCA. The advice about medication, exercise, long-term risk, family screening, follow-up, and prognosis may all change depending on the final diagnosis.
This is where modern cardiology is both powerful and nuanced. We have ECGs, blood tests, CT scans, angiograms, echocardiograms, cardiac MRI, genetic testing and more. None of these tests is perfect. None should be used thoughtlessly. But when used in the right patient, for the right reason, they can completely change the direction of care.
There is a temptation in medicine — and perhaps in life generally — to think in straight lines. Chest pain plus abnormal ECG plus raised troponin equals blocked artery. Often, that is true. But not always.
The job is to keep listening to the patient, follow the clues, use the right tests, and be prepared to change your mind when the evidence points somewhere else.
That is the power of testing: not simply to confirm what we already think, but sometimes to stop us being confidently wrong.