The case, published in BMC Psychiatry by a team led by Aditya Shrivastav of Datta Meghe Institute of Medical Sciences in India, is a striking real-world illustration of the nocebo effect — the dark twin of the placebo response, in which negative expectations about a treatment actively generate the very symptoms a patient fears. Where placebo heals through belief, nocebo harms through it. And in an era when anyone starting a medication can spend an evening scrolling through forums and horror stories about its side effects, researchers argue the phenomenon is quietly sabotaging mental health treatment on a massive scale.

The clinical picture the woman presented was genuinely alarming. She had been diagnosed with moderate major depressive disorder, and sertraline — a selective serotonin reuptake inhibitor, or SSRI — was a reasonable, guideline-consistent choice. But within two days of the first tablet, the cardiopulmonary storm began. Emergency physicians found sinus tachycardia, a racing but otherwise structurally normal heart rhythm, with no ischemic changes on the electrocardiogram to suggest the heart muscle was being starved of oxygen. Serial cardiac biomarkers, the proteins that spill into the bloodstream when heart tissue dies during a heart attack, remained stubbornly within normal limits. There was no clot, no arrhythmia crisis, no metabolic derangement to explain what she was feeling.

Then the imaging added a twist that kept the case from being dismissed. A transthoracic echocardiogram — an ultrasound of the beating heart — showed borderline left ventricular systolic function, with an ejection fraction of 51 percent, just under the conventional threshold of normal, accompanied by mild diffuse global hypokinesia, a subtle generalized weakening of the heart’s contraction. A brain MRI ruled out acute intracranial pathology. In other words, something real was measurable in her body, but nothing pointed to the acute cardiac catastrophe her symptoms seemed to announce. The team treated her supportively, and the symptoms gradually resolved — a pattern more consistent with a transient, expectation-driven physiological storm than with structural heart disease.

The detective work that followed is what elevates this from an oddity to a teaching case. When clinicians sat down with the patient for detailed psychiatric reassessment, a crucial piece of history emerged: before taking her first dose, she had immersed herself in online information about antidepressant adverse effects. And the symptoms she had read about — palpitations, chest tightness, breathlessness, dizziness — matched, with uncomfortable precision, the symptoms she then experienced. Her body had not simply malfunctioned. In a very real physiological sense, it had performed the script she had absorbed, translating anticipation of harm into autonomic arousal, hyperventilation, and cardiac symptoms indistinguishable from disease.

This is not metaphor; the nocebo effect has measurable biology. Expectation of a symptom activates the same neural circuitry that generates the symptom itself. Anticipatory anxiety drives sympathetic nervous system activation — adrenaline release, elevated heart rate, heightened interoceptive attention, the brain’s monitoring of internal bodily signals turned up to maximum gain. A person primed to detect palpitations will notice every benign flutter and interpret it as evidence of danger, which spikes anxiety further, which amplifies the sensation, in a self-reinforcing loop that can produce chest pain, hyperventilation, and genuine, measurable cardiovascular changes. The mind does not imagine the symptom. It manufactures it, through the same machinery that produces any other bodily experience.

What happened next is the part that should make every prescriber sit up. Rather than abandoning sertraline permanently — the fate of an estimated substantial fraction of patients who quit antidepressants in the first weeks because of early side effects — the team pursued a strategy of structured psychoeducation and expectation-targeted counselling. The patient was walked through what the medication actually does, what early effects are common and transient, and, critically, how expectation itself can generate symptoms. Then came the experiment that mattered: sertraline was reintroduced at a lower dose. This time, there was no recurrence of the cardiopulmonary symptoms. Same drug, same patient, same body — different expectations.

The five-week follow-up sealed the narrative. A repeat echocardiogram showed her left ventricular function had normalized entirely, with the ejection fraction rising to 58 percent. Her depression, measured on the 17-item Hamilton Depression Rating Scale, had fallen from 21 — firmly in the severe range — to 10, a substantial clinical improvement. The medication she had nearly lost to fear was, once fear was managed, doing exactly what it was prescribed to do. The authors are appropriately careful: a single case report cannot establish causality, and early genuine pharmacological effects of SSRIs cannot be completely excluded. But the absence of symptom recurrence after a psychoeducation-guided rechallenge is a powerful circumstantial fingerprint of an expectation-driven mechanism.

The broader implications reach well beyond one woman and one antidepressant. Adherence to psychiatric medication is a chronic, global problem, and the first two weeks of SSRI therapy are where most patients are lost — the window in which early side effects, real or expected, collide with a person who has not yet felt any benefit. The authors argue that recognition of nocebo phenomena, careful counselling, and proactive expectation management before the first tablet is swallowed could keep patients on effective treatment, spare emergency departments the cost of cascades of unnecessary cardiac workups, and prevent the premature discontinuation of medications that work. In an information environment where a search for any drug’s name surfaces its worst outcomes first, the prescription may increasingly need a companion: a conversation about what the internet has already told you, and what your own anticipating brain can do with it.

There is also a caution here for the rest of us, the patients rather than the prescribers. The case does not suggest symptoms are imaginary or that people should dismiss what their bodies tell them — this woman’s chest pain warranted a full emergency evaluation, and she received one, and that was the right call. What it suggests is that the mind is not a passive observer of pharmacology. It is a participant, sometimes a saboteur, capable of summoning the side effects it dreads most. The first dose of a medication, it turns out, is taken twice: once by the body, and once — often hours earlier, on a screen, in the dark — by the imagination. Only one of those doses comes with a dosage instruction.

Subject of Research: A nocebo effect case report in which expectation-driven cardiopulmonary symptoms after sertraline initiation mimicked acute cardiac pathology

Article Title: Nocebo-induced cardiopulmonary symptoms following sertraline initiation mimicking acute cardiac pathology: a case report

Article References: Shrivastav, A., Tivaskar, S., Luharia, A., & Mishra, G. (2026). Nocebo-induced cardiopulmonary symptoms following sertraline initiation mimicking acute cardiac pathology: a case report. BMC Psychiatry. https://doi.org/10.1186/s12888-026-08525-9

Image Credits: AI Generated

DOI: 10.1186/s12888-026-08525-9

Keywords: nocebo effect, sertraline, SSRI, placebo effect, major depressive disorder, cardiopulmonary symptoms, medication adherence, psychoeducation, treatment expectations, psychiatry, case report, antidepressants