参议员林赛·格雷厄姆因主动脉疾病去世。我的丈夫也是如此。


2026年7月13日 / 美国东部时间下午5:49 / 哥伦比亚广播公司新闻

参议员林赛·格雷厄姆于7月11日周六去世,享年71岁。验尸官的初步结论是主动脉夹层,即向心脏外输送血液的大动脉主动脉壁出现撕裂。最终死亡证明仍在等待出具。多数报道称其死因为“突发性”。主动脉疾病通常在出现撕裂或破裂前没有任何症状。

主动脉可能出现的问题

主动脉是人体最大的动脉,从心脏出发向下贯穿胸腔和腹腔。它可能出现三种不同的病变。三者虽相关但并不相同,而且经常被混淆。

动脉瘤是血管壁的膨出。主动脉壁的薄弱区域逐渐拉伸并向外形成囊状凸起。这种病变发展缓慢,通常需要数年时间,且通常不会引发症状,这也是大多数动脉瘤都是在因其他原因进行扫描时偶然被发现的原因。动脉瘤以尺寸大小作为判定标准。血管扩张得越宽,管壁就越薄、越脆弱,最终破裂的风险也就越高。

由Gemini Nano Banana Pro / 塞琳·贡德里博士制作的插图

主动脉夹层是血管壁撕裂。血液突破内层内膜,涌入血管壁内部,将各层分离并形成假腔。这种病变是突发性的真正急症,通常以突发的、撕裂样的胸部或背部疼痛为标志性症状。它并非一定由动脉瘤引发。夹层可能发生在从未扩张过的主动脉上,这也是它经常被漏诊的原因之一。

主动脉破裂是血管壁完全破损。血管壁彻底破裂,血液涌入不该出现的区域,进入胸腔或心脏周围的心包腔。这通常是致命的结局,动脉瘤或夹层都可能发展至此,且可能在数分钟内致人死亡。

由Gemini Nano Banana Pro / 塞琳·贡德里博士制作的表格

膨出、撕裂、破裂。一种病变可能引发另一种,但三者并不相同。夹层更偏好攻击老年人,由高血压和动脉粥样硬化引发。年轻人的动脉瘤则更可能是遗传性的,由结缔组织本身的缺陷导致。

这种区别正是格雷厄姆和我丈夫的不同之处。71岁的格雷厄姆的主动脉出现撕裂,也就是夹层,其血管壁因验尸官所称的动脉粥样硬化性心血管疾病而僵硬了数十年。我的丈夫格兰特·瓦尔则是血管膨出后破裂,他去世时的年龄,这类疾病通常意味着存在遗传性病因。

格雷厄姆所患的是常见类型,由年龄、高血压和动脉粥样硬化引发。对大多数人来说,这并不意味着需要专门去筛查动脉瘤。但这提醒我们要控制好血压,也提醒急诊室要将主动脉撕裂纳入鉴别诊断清单,因为它仍经常被误诊为心脏病发作。目前在这类疾病中,唯一经过验证的筛查项目是:对65至75岁有吸烟史的男性进行一次性腹部超声检查,以筛查腹主动脉瘤。除此之外,几乎所有看到这篇文章的人都不需要明天就去做扫描。

夺走我丈夫生命的是另一种类型的主动脉疾病,它并不遵循上述规律。这种疾病具有家族遗传性,发病年龄早数十年,且通常在动脉破裂前没有任何预警信号。常规体检无法发现它,也没有针对该类疾病的全民筛查项目。大多数家庭都是在有人去世后才意识到自己携带了这种致病风险,就像我们家一样。这并不是让所有人都陷入恐慌的理由。但如果主动脉疾病在你的家族中存在,就可以通过影像检查,有时还可以通过基因检测在病情变得危险之前及早发现。

无人察觉的动脉瘤

2022年12月,我的丈夫、足球记者格兰特·瓦尔在卡塔尔报道世界杯四分之一决赛时,在新闻发布厅内晕倒。当晚他就去世了,年仅49岁。

动脉瘤位于心脏上方的第一段主动脉,直径达6.0厘米,破裂后血液充满了他的心包腔。尸检发现,他的血管壁内部已经缓慢变薄,弹性纤维出现断裂。他的动脉几乎没有出现硬化。他的情况是,一名50岁以下的男性出现动脉瘤并破裂,不存在导致参议员死亡的数十年动脉老化问题。

我为何要求尸检

我是一名医生、流行病学家和医学记者。我的工作就是调查。我习惯于从机制和证据的角度思考问题,不会接受“他死于突发疾病”作为最终结论。因此,我向纽约市验尸官办公室申请了全面尸检。我想知道究竟发生了什么,寻求一个合理的解释。我是否遗漏了什么?有没有什么措施可以预防或治疗这种疾病?导致他死亡的病因能否用于保护格兰特的其他家人,或是帮助其他家庭?我需要弄清楚这一切。悲伤会让你反复回想每一个平凡的日子,寻找自己当时没能察觉的迹象,而尸检给了我答案,而非让我陷入无休止的自我追问。它给了我解脱,具有治疗意义。

同时,尸检也为我另一个更残酷的目的提供了事实依据。在格兰特去世后的几天内,那些散布疫苗错误信息的人声称新冠疫苗导致了他的死亡。尸检结果明确无误:他的病毒检测呈阴性,报告明确指出他之前接种的疫苗“既没有引发也没有促成”动脉瘤破裂。我已经在其他地方写过相关内容,这里就不再赘述。

尸检在他的DNA中发现的线索

纽约市验尸官办公室拥有全美唯一一家设于验尸官办公室内的分子遗传学实验室。该实验室对猝死人群的DNA进行检测,每年约处理500起案件,其中约100起能找到遗传病因。在格兰特的心脏组织中,实验室发现了FBN1基因的变异,该基因与马凡综合征相关。

格兰特并没有患马凡综合征。他身材高挑,但并不符合马凡综合征的诊断标准。他只是在一个帮助构建维持主动脉壁的结缔组织的基因上出现了一处单核苷酸变异,实验室将其归类为“意义未明的变异”。我们无法确定这个变异就是导致他患上动脉瘤的原因。但这是最有可能的解释,而且遗传性结缔组织疾病已被证实是60岁以下人群患上升主动脉动脉瘤的风险因素。

甄别哪些变异确实会致病是一项尚未完成的工作。休斯顿德克萨斯大学健康科学中心的戴安娜·米莱维茨博士团队多年来一直在绘制胸主动脉疾病相关基因图谱。其他研究团队则在研究相反的问题:为什么有些人携带马凡综合征突变却从未发病,寻找似乎能保护主动脉的“修饰基因”。格兰特的变异就处于这种不确定性之中。

将死亡转化为预防手段

这种不确定性并未改变后续的行动。一旦实验室确认了该变异,格兰特的血亲就可以接受针对该特定变异的检测。我的姐夫埃里克,也就是格兰特的兄弟,携带了该变异。他的叔叔、一个侄女、一个侄子以及其他家庭成员也都接受了检测。埃里克还接受了超声心动图、核磁共振和CT扫描。他的主动脉结构正常。他现在会定期接受影像检查,如果他的主动脉开始扩张,医生就能提前发现,从而有多年时间采取干预措施。

这就是尸检的意义所在。它让那些与格兰特共享DNA的亲属获得了可以采取行动的依据。

同样死于这类疾病的还有演员约翰·里特。2003年,54岁的他死于主动脉夹层,却被误诊为心脏病发作。他的遗孀艾米·亚贝克创立了约翰·里特主动脉健康基金会,为米莱维茨的研究项目提供资金支持,目前已招募了超过1500个家庭参与相关研究。埃里克现在也在该基金会进行宣传工作。里特去世23年后,主动脉夹层在急诊室仍经常被误诊,因为它的症状与心脏病发作相似,而且大多数临床医生并不会考虑到这种可能。

但这不仅仅是患者需要为自己发声。临床医生在让患者出院前,应该先考虑主动脉撕裂的可能性,遗传学家也可以在猝死事件后对家属进行检测。纽约市验尸官办公室最近推出了一项名为GIFTS的项目,为死于遗传性疾病的死者的在世亲属提供免费基因检测,这是全美首次由验尸官办公室为在世患者提供此类检测。该实验室主任唐莹莹博士告诉我,这个项目的设立正是受到了像我们家这样的家属的启发。

你应该去做检查吗?

我经常被问到两个问题:

出现哪些情况应该去做筛查? 一级亲属,即父母、兄弟姐妹或子女,患有胸主动脉瘤或夹层,或家族中有不明原因的猝死事件,尤其是在60岁之前发生的。同时出现结缔组织疾病的身体特征:身材异常高挑、四肢修长、胸骨凹陷或突出、重度近视或晶状体脱位。当前的心脏病学指南建议,对任何患有胸主动脉疾病患者的一级亲属进行主动脉影像检查。

还有一种情况与家族病史无关:65至75岁有吸烟史的男性,应接受一次性腹部超声检查,筛查腹主动脉瘤。如果你属于这个群体,请向医生提出检查要求。

谁应该接受基因检测? 患有胸主动脉瘤或夹层,同时伴有结缔组织疾病特征、有主动脉疾病家族史,或在60岁前发病的人群。当发现致病变异后,家族其他成员可以接受针对该特定变异的检测。通过这种方式,就能找到像埃里克这样携带风险但主动脉尚未出现异常的人。

如果发现了动脉瘤该怎么办?确诊的动脉瘤是一种可控的疾病:控制血压、定期进行影像检查,当尺寸达到阈值时进行手术。升主动脉的手术阈值约为5.5厘米,遗传性病例的阈值更低。格兰特的动脉瘤直径为6.0厘米,早已达到修复标准。但当时没有人发现这一点。

我当时不可能提前发现。他没有任何症状,生活中也没有任何迹象能让医生怀疑他的主动脉存在问题。但很多家庭可以做到。如果你的直系亲属曾被主动脉疾病影响,请向医生咨询影像检查,以及基因检测是否对你有意义。

_本文最初发表于塞琳·贡德里博士的《潜在病症》Substack新闻通讯。_点击此处阅读更多内容并订阅。

Senator Lindsey Graham just died of aorta disease. My husband did too.

July 13, 2026 / 5:49 PM EDT / CBS News

Senator Lindsey Graham died on Saturday, July 11th, at 71. The medical examiner’s preliminary finding was an aortic dissection, a tear in the wall of the aorta, the large artery that carries blood out of the heart. The final death certificate is still pending. Most of the coverage called it “sudden.” Aortic disease is usually silent until it tears or bursts.

What can go wrong in the aorta

The aorta is the body’s largest artery, running from the heart down through the chest and abdomen. Three different things can go wrong with it. They’re related but not the same, and they get confused all the time.

An aneurysm is a bulge. A weak spot in the aortic wall stretches and balloons outward. It happens slowly, over years, and usually causes no symptoms, which is why most aneurysms are found by accident on a scan done for something else. An aneurysm is defined by size. The wider it grows, the thinner and more fragile the wall gets, and the higher the odds that it will eventually fail.

Illustration created with Gemini Nano Banana Pro / Dr. Céline Gounder

A dissection is a tear. Blood breaks through the inner lining and forces its way into the wall itself, splitting the layers apart and carving a false channel. This one is sudden and is a true emergency, usually announced by abrupt, tearing chest or back pain. It doesn’t require an aneurysm first. A dissection can strike an aorta that was never enlarged, which is part of why it gets missed.

A rupture is a burst. The wall gives way completely, and blood pulses out where it shouldn’t, into the chest or the sac around the heart. It’s the usually fatal ending that either an aneurysm or a dissection can lead to, and it can kill in minutes.

Table created with Gemini Nano Banana Pro / Dr. Céline Gounder

Bulge, tear, burst. One can set off another, but they aren’t the same. Dissection skews older, driven by high blood pressure and hardened arteries. An aneurysm in a younger person is more likely to be inherited, caused by a weakness in the connective tissue itself.

That difference is what separated Graham from my husband. Graham’s aorta, at 71, tore, a dissection along a wall stiffened by decades of what the medical examiner called arteriosclerotic cardiovascular disease. My husband Grant Wahl’s bulged and burst, at an age when this disease usually means something inherited.

Graham’s kind is the common one, driven by age, blood pressure, and hardened arteries. For most people, it isn’t a reason to go hunting for an aneurysm. It’s a reason to treat your blood pressure and for emergency rooms to keep a tear in the aorta on their radar, because it still gets mistaken for a heart attack. There is one proven screening test in this whole area: a one-time ultrasound for men 65 to 75 who have ever smoked, which looks for abdominal aneurysms. Beyond that group, almost no one reading this needs a scan tomorrow.

The version that killed my husband is the other one, and it doesn’t play by those rules. It runs in families, it strikes decades earlier, and it usually gives no warning until the artery fails. A routine checkup won’t find it, and no population screening program looks for it. Most families learn they carry it the way mine did, after someone dies. None of this is a reason for everyone to panic. But if aortic disease runs in your family, it can be caught early, with imaging and sometimes genetic testing, long before it turns dangerous.

The aneurysm nobody saw

In December 2022, my husband, the soccer journalist Grant Wahl, collapsed in the press box while covering a World Cup quarterfinal in Qatar. He died that night. He was 49.

The aneurysm was in the first stretch of aorta just above his heart, 6.0 cm across, and when it ruptured it filled the sac around his heart with blood. The autopsy found the wall had been thinning from the inside for a long time, its elastic fibers fragmenting. There was almost no hardening of his arteries at all. His was a bulge that burst in a man under 50, without the decades of arterial wear that killed the senator.

Why I asked for an autopsy

I’m a physician, epidemiologist, and medical journalist. I investigate. I think in terms of mechanisms and evidence, and I don’t accept “he died suddenly” as a stopping point. So I asked the New York City medical examiner for a full autopsy. I wanted to know what had happened, and I wanted an explanation. Had I missed something? Could anything have been done to prevent it or treat it? Could whatever killed him be used to protect the rest of Grant’s family, or help other families? I needed to make sense of it. Grief leaves you turning every ordinary day over, looking for the sign you didn’t catch, and the autopsy gave me answers instead of that loop. It gave me closure. It was therapeutic.

It gave me facts I needed for an uglier reason, too. Within days of Grant’s death, people invested in vaccine disinformation claimed the COVID shot had killed him. The autopsy was unambiguous: he tested negative for the virus, and the report stated that his prior vaccination “neither caused nor contributed” to the rupture. I’ve written about that elsewhere, and I’ll leave it there.

What the autopsy found in his DNA

The New York City medical examiner’s office runs the only molecular genetics laboratory housed inside a medical examiner’s office in the country. It tests the DNA of people who die suddenly, reviewing about 500 cases a year and finding a genetic cause in roughly 100 of them. In Grant’s heart tissue, the lab found a variant in FBN1, the gene behind Marfan syndrome.

Grant did not have Marfan. He was tall, but he didn’t have the syndrome. What he had was a single change in a gene that helps build the connective tissue holding the aortic wall together, in a spot the labs classify as a “variant of uncertain significance.” We don’t know for certain that this variant caused his aneurysm. It’s the most likely explanation, and inherited connective tissue problems are well-established risk factors for ascending aortic aneurysms in people under 60.

Sorting out which of these variants actually cause disease is real, unfinished work. Dr. Dianna Milewicz’s group at UTHealth Houston has spent years mapping the genes behind thoracic aortic disease. Other teams are chasing the opposite question: why some people carry a Marfan mutation and never get sick, hunting “modifier” genes that seem to shield the aorta. Grant’s variant sits inside that uncertainty.

Turning a death into prevention

None of that uncertainty changed what came next. Once the lab identified the variant, Grant’s blood relatives could be tested for that exact change. My brother-in-law Eric, Grant’s brother, carries it. His uncle, a niece and a nephew, and other family members have been tested, too. Eric had echocardiograms as well as MRI and CT scans. His aorta is structurally normal. He now gets regular imaging, and if his aorta ever starts to enlarge, his doctors will see it coming, with years to act.

That’s what the autopsy did. It gave the people who share Grant’s DNA something they could act on.

The same disease killed the actor John Ritter. In 2003, at 54, he died of an aortic dissection that was mistaken for a heart attack. His widow, Amy Yasbeck, started the John Ritter Foundation for Aortic Health, which funds Milewicz’s research program and has enrolled more than 1,500 families. Eric now advocates with them. Twenty-three years after Ritter’s death, aortic dissection is still routinely missed in emergency rooms because it mimics a heart attack and most clinicians aren’t thinking about it.

But it’s not just for patients to advocate for themselves. Clinicians should consider a tear in the aorta before sending someone home, and geneticists can test families after a sudden death. The New York City medical examiner recently launched a program called GIFTS that offers free genetic testing to the living relatives of people who died of inherited conditions, the first time a medical examiner’s office has tested living patients. The lab’s director, Dr. Yingying Tang, told me the program was shaped by families like mine.

Should you get checked?

Two questions I get asked a lot:

What should prompt you to get screened?A first-degree relative, a parent, sibling, or child, with a thoracic aortic aneurysm or dissection, or a sudden unexplained death in the family, especially before 60. Physical features of a connective tissue disorder: being very tall with long limbs, a chest that caves in or juts out, severe nearsightedness, or a dislocated lens. The current cardiology guidelines recommend imaging the aorta in the first-degree relatives of anyone with thoracic aortic disease.

One more, and it has nothing to do with family history: men 65 to 75 who have ever smoked should get a one-time abdominal ultrasound to check for an abdominal aortic aneurysm. If that’s you, ask your doctor for it.

Who should get genetic testing?People with a thoracic aortic aneurysm or dissection who also have features of a connective tissue disease, a family history of aortic disease, or disease before 60. When a disease-causing variant turns up, the rest of the family can be tested for that exact variant. That’s how you find the Eric’s, the ones carrying the risk whose aortas are still normal.

And if an aneurysm is found? A known aneurysm is a manageable condition: blood pressure control, regular imaging, and surgery once it reaches a size threshold, around 5.5 cm for the ascending aorta and lower for people with genetic forms. Grant’s was 6.0 cm, well into repair territory. Nobody knew it was there.

I couldn’t have known. He had no symptoms, and nothing in his life would have pointed a doctor to his aorta. But a lot of families can know. If aortic disease has touched your blood relatives, ask your doctor about imaging and ask whether genetic testing makes sense for you.

_This article was originally published in_Dr. Céline Gounder’s “Underlying Conditions”_newsletter on Substack._Read more and subscribe here.

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