雅思阅读 163: The Inflammatory Battlefield Within Our Arteries（动脉内部的炎症战场）

改编自 Scientific American（2026年4月）。雅思阅读 Section 3 难度，约 1050 词。 素材来源：https://www.scientificamerican.com/article/new-evidence-links-heart-disease-to-inflammation-and-drugs-can-stop-it/

Reading Passage

A. Heart disease kills more people in the United States than any other illness, and cardiologists have, for decades, been drilled to watch a fearsome foursome of culprits: raised blood pressure, tobacco smoking, elevated "bad" LDL cholesterol and type 2 diabetes. Yet a stubborn anomaly has shadowed this tidy picture all along. A substantial fraction of the patients admitted to hospital after a heart attack exhibit none of these four classic hazards, and, paradoxically, these so-called "low-risk" patients tend to fare worse than those carrying obvious risk factors. A 2023 analysis of acute coronary cases found that individuals with none of the four risks were 57 percent more likely to die than patients presenting with at least one. Roughly a quarter of heart-attack victims, in other words, collapse for reasons the standard checklist cannot explain, and many of them carry what clinicians dismissively call "ideal" cholesterol readings. Translated into numbers, of the roughly 920,000 Americans who succumb to cardiovascular disease each year, about 230,000 do so with no obvious cause. Even more puzzling, follow-up studies suggest these anomaly patients tend to die sooner, not later, than the textbook cases, as if the very factor that blinds the risk checklist also makes the disease more aggressive. This unexplained quarter has long nagged at Paul Ridker, a preventive cardiologist at Brigham and Women's Hospital in Boston, who recalls concluding that some fundamental determinant of disease must be missing from the textbooks. For him, the gap between what statistics predicted and what the wards actually saw was not a footnote but a scientific scandal.

B. The missing piece, Ridker and a growing band of collaborators now argue, is chronic inflammation — a prolonged, body-damaging state of immune activation. The orthodox view once held that atherosclerosis, the gradual buildup of fatty material on artery walls, was a passive and almost mechanical process, an inevitable by-product of ageing comparable to rust accumulating inside a pipe. A closer look suggests otherwise. When cholesterol accumulates in an artery, it can crystallise into sharp, needle-like formations that the immune system no longer recognise as self; the body then mobilises white blood cells to attack the intruder, and in doing so tears at the very vessel lining it was meant to protect. The battle leaves behind a roughened, unstable plaque that can suddenly rupture and trigger a clot. Hints of this mechanism are far older than modern medicine: in the 1850s the German pathologist Rudolf Virchow peered through his microscope and saw angry, inflamed tissue within diseased arteries, and in 1913 the Russian researcher Nikolai Anichkov noticed arteries of cholesterol-fed rabbits teeming with white blood cells. For decades, though, most readers assumed inflammation merely followed the damage, a kind of secondary redness on already injured tissue, rather than being the engine itself. The distinction matters enormously: if inflammation is a bystander, suppressing it is pointless; if it is a driver, calming it could interrupt the disease long before a fatal plaque ever forms.

C. The turning point came from epidemiology. In the mid-1990s Ridker's team drew on the Physicians' Health Study, which had tracked male doctors since 1982, and measured blood levels of C-reactive protein (CRP), a molecular "flare" that signals inflammation. Comparing 543 doctors who later suffered a heart attack, stroke or severe clot with 543 who remained event-free, the researchers found that those with the highest CRP readings were three times as likely to suffer a heart attack and twice as likely to suffer a stroke as men with the lowest readings. A parallel investigation of nearly 28,000 women in the Women's Health Study, followed for an average of eight years, delivered a similar verdict: the most inflamed fifth of participants faced a 2.3-fold greater chance of a serious cardiac event than the least inflamed. Such dose-response patterns argued that inflammation was no mere side effect but a lethal accomplice, and that the risk rose smoothly as the marker climbed. A further clue came unexpectedly from statins, the cholesterol-lowering drugs that already formed the backbone of prevention: careful analyses hinted they protected users partly beyond simply lowering LDL, as if they also damped the immune system in passing. In 1999 the pathologist Russell Ross declared in a leading journal that "atherosclerosis is clearly an inflammatory disease", a judgement that mountains of subsequent data, drawn from hundreds of thousands of patients, have gone on to confirm.

D. If inflammation accelerates disease, then damping it down might protect the heart — a leap that required proof. The decisive evidence arrived with a large randomised trial called CANTOS, in which an antibody drug that blocks a key inflammatory molecule cut cardiovascular events by a modest but significant amount among patients already on cholesterol-lowering statins, though it also raised the risk of certain infections. More clinically influential was the reuse of colchicine, an inexpensive medicine long prescribed for gout: a 2020 trial showed it reduced heart attacks, strokes and related complications by roughly 31 percent, largely in patients already taking statins, and in June 2023 regulators approved it for that purpose. Not every study has reproduced the benefit, however, and some cardiologists remain wary of switching on anti-inflammatory treatment broadly, lest they blunt the very immune defences people need against infection. The CANTOS antibody, for instance, lowered heart attacks slightly but noticeably increased deaths from deadly infections, a reminder that inflammation is a double-edged system the body uses to repel bacteria as well as to build plaques.

E. The controversy itself reveals how thoroughly the field has shifted. The American College of Cardiology recommended, in the autumn of 2025, that clinicians routinely screen patients for inflammatory proteins, a practice once considered eccentric. Researchers are now testing more precise anti-inflammatory agents aimed at particular molecular pathways, hoping to gain benefit without weakening immunity. The deeper change is conceptual: the vascular system is no longer imagined as a network of slowly clogging pipes but as a series of contested battlefields where an overzealous immune reaction inflicts as much harm as the cholesterol it is reacting to. Whether that reframing will, as its advocates predict, save millions of lives, depends on sorting which patients genuinely benefit from anti-inflammatory drugs — a task that, like the original puzzle itself, the old risk-factor checklist alone cannot solve.

Questions 1-4

Choose the correct heading for paragraphs B, C, D and E from the list of headings below.

List of Headings i. The hidden culprit behind the clogged-pipe metaphor ii. A historical survey of surgical techniques iii. Blood tests that linked inflammation to later events iv. The commercial value of pharmaceutical patents v. Drugs designed to calm the immune system vi. Why cholesterol is harmful to the liver vii. A field transformed — and questions that remain

1. Paragraph B: ____
2. Paragraph C: ____
3. Paragraph D: ____
4. Paragraph E: ____

Questions 5-8

Choose the correct letter, A, B, C or D.

5. What is surprising about the "low-risk" heart-attack patients? A. They are younger than other patients. B. They tend to have worse outcomes despite lacking classic risk factors. C. They smoke more than other patients. D. They recover faster than expected.

6. According to the writer, what happens when cholesterol crystallises? A. It dissolves harmlessly in the bloodstream. B. It triggers an immune attack that damages the artery lining. C. It directly lowers blood pressure. D. It is absorbed by healthy cells without a reaction.

7. What did Ridker's analysis of C-reactive protein show? A. High CRP predicted a higher chance of later cardiac events. B. CRP levels were unrelated to heart attacks. C. Only women had raised CRP. D. CRP is produced by the liver exclusively.

8. Why are some cardiologists reluctant to prescribe anti-inflammatory drugs? A. They are too expensive to manufacture. B. They may weaken the body's ability to fight infection. C. They have never reduced any events in trials. D. They work only on patients under 40.

Questions 9-13

Do the following statements agree with the claims of the writer?

Write:

• TRUE if the statement agrees with the information
• FALSE if the statement contradicts the information
• NOT GIVEN if there is no information on this

9. Roughly a quarter of heart-attack patients lack all four classic risk factors.
10. Rudolf Virchow was the first to prove that inflammation causes atherosclerosis.
11. In the Women's Health Study, women with the highest CRP were followed for eight years on average.
12. Colchicine was originally developed specifically to treat heart disease.
13. The American College of Cardiology has recommended screening for inflammatory proteins.

Questions 14-15

Complete the summary below using NO MORE THAN TWO WORDS from the passage.

For decades atherosclerosis was seen as a passive process, much like (14) __________ accumulating inside a pipe. Modern research instead portrays artery walls as contested (15) __________ where an overactive immune reaction inflicts damage.

答案与解析

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