Alcoholic Cardiomyopathy Deaths Fell for 25 Years. The Early 2020s Interrupted That.

Between 1999 and 2024, deaths from most forms of cardiomyopathy in the United States fell steeply. The rate for dilated cardiomyopathy dropped by nearly two-thirds. The catch-all "unspecified" category fell by more than half. Hypertrophic cardiomyopathy slid by half. Then there is alcoholic cardiomyopathy — the subtype tied directly to sustained heavy drinking — which declined by a little over a quarter and, in the middle of the study window, moved in the opposite direction.

That divergence is the central finding of a Cureus analysis published October 4, built from a quarter-century of CDC death-certificate records. It is a study of mortality codes rather than patients, and its authors say so repeatedly. The pattern still holds: while most heart-muscle deaths became rarer, the alcohol-linked version resisted the trend, and it resisted it hardest among the middle-aged men and the regions already carrying the heaviest drinking burden.

Twenty-Five Years of Death Certificates

The team ran a serial cross-sectional analysis of the CDC's Wide-ranging Online Data for Epidemiologic Research (WONDER) underlying-cause-of-death file, spanning 1999 through 2024. Cardiomyopathy deaths were pulled using a set of ICD-10 codes covering dilated, obstructive and other hypertrophic, restrictive, alcoholic, and unspecified disease. The researchers recalculated annual age-adjusted mortality rates (AAMRs) by sex, and crude death rates across three age bands — 15 to 44, 45 to 64, and 65 to 84 — then broke alcoholic cardiomyopathy out by race and by state.

The headline numbers describe genuine progress. Dilated cardiomyopathy fell from 1.965 deaths per 100,000 to 0.716, a 63.6 percent decline. Unspecified cardiomyopathy — the largest category by volume — fell from 7.196 to 3.155, down 56.2 percent. Other hypertrophic cardiomyopathy dropped 49.2 percent, and the obstructive subtype 33.4 percent. A small "other restrictive" category held essentially flat.

Alcoholic cardiomyopathy declined too, but only from 0.199 to 0.144 per 100,000, a 27.7 percent reduction. It is the second-smallest improvement of any subtype the study tracked, and the only one whose rate climbed and then fell within the observation window. The authors place it plainly: "ACM showed a smaller endpoint reduction than dilated, unspecified, and other hypertrophic cardiomyopathy and an increase during the early 2020s before declining in 2023-2024."

The Spike That Overlapped a Drinking Surge

The early-2020s rise did not happen in a vacuum. During roughly the same stretch, deaths attributable to excessive alcohol use in the United States rose 29.3 percent — from an average of 137,927 a year in 2016-2017 to 178,307 in 2020-2021 — with the age-standardized mortality rate climbing from 38.1 to 47.6 per 100,000. Survey data documented parallel shifts in drinking behavior and its consequences through the pandemic years.

The study is explicit that this is correlation, not causation. Individual alcohol exposure, healthcare use, and treatment history were not available in the death records, so the observed overlap "cannot establish causality," the authors write. The honest reading is that a population-level surge in drinking coincided with a subtype-specific mortality bump, and that the bump is at least consistent with the exposure data rather than contradicting it.

A Fourfold Gap That Cuts Both Ways

Men accounted for most of the burden and most of the improvement. Male alcoholic cardiomyopathy mortality fell from an AAMR of 0.408 to 0.209 — a 48.8 percent decline — while the female rate rose slightly, from 0.047 to 0.054, a 15.9 percent increase off a very low base. Despite the male improvement, the 2024 male rate remained nearly four times the female rate.

Age-specific figures localize the risk further. Among men, crude death rates fell in every band: 0.16 to 0.10 for ages 15 to 44, 0.89 to 0.47 for 45 to 64, and 1.03 to 0.57 for 65 to 84. Among women, rates held roughly steady in the two younger bands, but the 65-to-84 rate climbed from 0.09 to 0.11 per 100,000.

It would be a mistake to read the female numbers as evidence that women are biologically protected. The study's own discussion rejects that inference. Women can develop alcohol-related cardiovascular harm at lower levels of exposure than men, and binge-drinking prevalence among adults aged 18 to 25 actually flipped during the study period: women trailed men in 2017-2019, then exceeded them in 2021-2023. Because alcoholic cardiomyopathy reflects years of cumulative exposure, those changing patterns may simply not have had time to surface in mortality data. The low absolute female rate is the kind of figure that lulls a system into not screening.

For anyone working with alcohol use disorder, the practical signal is that cardiac risk is not confined to the patient profile clinicians picture — the older, male, long-term heavy drinker — even if that profile still accounts for the largest share of deaths.

Alaska Was Highest. Five States Got Worse.

State-level results show wide geographic spread that national averages conceal. Pooled for 2018-2024, Alaska had the highest rate of any state, 1.342 per 100,000, up sharply from 0.651 a decade earlier. Five other states posted higher pooled rates in the later period than the earlier one: Utah (0.248 versus 0.074), Oregon (0.368 versus 0.222), Tennessee (0.280 versus 0.179), Iowa (0.290 versus 0.198), and Washington (0.336 versus 0.259).

Why Geography Isn't Destiny

The authors are careful here, and the caution is warranted. The state comparison stacks two pooled periods rather than tracking continuous trends, estimates from small states can be unstable, and the District of Columbia's later-period figure was suppressed entirely. The mechanisms behind the differences cannot be recovered from death certificates; they may reflect alcohol exposure, population makeup, socioeconomic and healthcare factors, or even variation in how deaths get coded. The study labels the geographic findings "hypothesis-generating," which is the right word for a pattern that deserves follow-up rather than a conclusion.

Declines, meanwhile, were concentrated in states including New Jersey, California, North Carolina, Virginia, and New York.

Race, Absolute Burden, and a Coding Caveat

American Indian and Alaska Native individuals recorded the highest race-specific rates in both periods, 0.6 per 100,000, with Black or African American and White rates each measuring around 0.2 in 2018-2024. The authors stress that these are not biological distinctions; prior research shows alcohol-attributable mortality disparities persist even after accounting for differences in consumption, pointing instead to social determinants and unequal access to treatment. They also flag that racial misclassification on death certificates likely understates mortality among AI/AN populations.

Absolute counts tell a different story than rates. White individuals accounted for the largest number of alcoholic cardiomyopathy deaths in both periods — 7,282, or 77.9 percent of the total, from 1999-2017, and 3,306 in 2018-2024. Rates describe who is most at risk per capita; counts describe where the largest volume of loss sits. Both matter for how prevention money gets spent.

The Problem With a Narrow Organ — and What It Means for Treatment

There is a temptation to treat alcoholic cardiomyopathy as a specialist's concern, a cardiology footnote to the addiction field. The October 2 HCPLive hepatology report on alcohol-associated liver disease points in a similar direction from another organ: as U.S. drinking trends downward overall, heavy drinking among adults aged 50 to 64 is still rising, and alcohol-related organ damage may lag the exposure curve by years. The two conditions share a driver and a blind spot — a healthcare system organized around organs rather than around drinking.

The cardiomyopathy study's concluding recommendation follows that logic. It calls alcoholic cardiomyopathy a "potentially modifiable" burden and argues for closer integration of cardiovascular prevention and heart-failure care with systematic alcohol assessment and evidence-based treatment of alcohol use disorder. In plain terms: the cardiologist should be asking about drinking, and the treatment system should be expecting the cardiac patient.

No part of this analysis suggests that abstaining or cutting back is futile — the 27.7 percent decline is real, and it happened over a period when treatment access expanded. It suggests that the intervention window is wider than a single specialty. Alcohol use disorder has three FDA-approved medications, including naltrexone and acamprosate, and the evidence for combining medication with behavioral care is stronger than for either alone. A patient whose first alcohol-related crisis is a heart-failure admission is still a candidate for that treatment; the goal should be catching them before the admission.

What the Study Can't Tell Us

Several limits are worth stating without softening. This is a descriptive analysis built on death certificates, and the authors ran no formal statistical tests for trend differences, so the divergent trajectories should be read as observed patterns, not proven distinctions. It cannot say how much any individual drank, whether they were ever offered treatment, or how many deaths were misattributed. Cause-of-death coding for cardiac events is imperfect, and the study cannot separate people who drank heavily for decades from those with brief but intense exposure late in life.

What it can do is put a number on a slow-moving harm that rarely makes headlines, and show that the number is not improving as fast as its neighbors. That gap — between a heart condition the country is beating and one it is not — is the finding worth carrying forward.