2Cardiovascular Disease and Hypertension

FHow the cardiovascular system reaches the ear

The cochlea is one of the most metabolically demanding structures in the body and depends on a steady, end-arterial blood supply with little collateral reserve. Anything that disturbs that supply — pressure, flow, or the vessel wall itself — can register as sound. Cardiovascular disease does this in three broad ways: it makes blood flow turbulent and audible, it transmits sounds generated in the heart and great vessels, and it reduces or destabilises cochlear perfusion [2003].

When the audible result beats in time with the heart, we call it pulsatile tinnitus, and it is the cardiovascular system’s most characteristic auditory signature. A continuous, non-rhythmic tinnitus can also arise when chronic vascular disease quietly injures the cochlea over years [2013].

THypertension and tinnitus

Hypertension is the most prevalent cardiovascular contributor a tinnitus clinic will meet. Large cross-sectional data show that hypertensive status — and the severity of the hypertension — is associated with a higher burden of tinnitus, and a STROBE-compliant analysis has linked systemic arterial hypertension with both tinnitus and hearing loss [2026][2026]. The proposed mechanisms include endothelial dysfunction, arteriolar stiffening, and impaired cochlear microcirculation, alongside a contribution from the antihypertensive drugs themselves.

The practical message is hopeful: because blood pressure is modifiable, optimising control is a legitimate part of tinnitus management in a hypertensive patient, not merely general health advice. It should be pursued deliberately, with the tinnitus tracked as one of the outcomes.

TAtherosclerosis, carotid disease and the wider cardiovascular burden

Atherosclerotic disease of the carotid and vertebrobasilar vessels can produce pulsatile tinnitus directly, through turbulent flow across a stenosis or an irregular, tortuous vessel lying close to the temporal bone. Markers of atherogenic risk track with tinnitus in population data — for example, the atherogenic index of plasma has been associated with tinnitus in NHANES-based analysis [2025]. Population cohorts have also examined whether tinnitus signals broader cardiovascular risk: the Tromsø Study explored the link between tinnitus and cardiovascular disease at a community level [2024], and a separate analysis examined tinnitus and the risk of cardiovascular events and all-cause mortality [2024].

The evidence is associative rather than uniformly causal, and some studies find no independent link — but the consistent clinical lesson is that a patient with pulsatile tinnitus and vascular risk factors deserves a vascular work-up rather than reassurance alone.

CHigh-output states and transmitted murmurs

Even with normal vessels, a heart that is pumping hard can make the ears ring. High-output states — anaemia, thyrotoxicosis, pregnancy, arteriovenous fistulae — raise flow velocity throughout the circulation, and the resulting hyperdynamic turbulence can become audible as pulsatile tinnitus. The clue is that treating the high-output state, not the ear, resolves the sound.

A distinct mechanism is transmission: a valvular murmur or a great-vessel bruit can be conducted up to the cochlea and heard by the patient. This is where the stethoscope earns its place in the tinnitus clinic — auscultation of the neck, periauricular region, and praecordium can identify a transmitted cardiac sound and redirect the entire work-up. Contemporary assessment of pulsatile tinnitus is built around exactly this kind of systematic listening and targeted imaging [2011][2014].