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Can You Train With a Heart Murmur? The Sound-Is-Not-the-Verdict Audit: The Door Where Both of the Gym's Default Scripts — a Murmur Means Your Heart Can't Take Strain, So No Lifting and No Hard Cardio, and Everyone Has One, It's Nothing, Train Through Whatever You Feel — Fail the Reader (the Community Column: Framingham's 3,491 — MVP Is 2–3% Prevalent and Far More Benign Than Referral Series Ever Suggested, Severe Regurgitation in Just 6.5% of Classic MVP; the Tail Column: the Arrhythmic-MVP Sudden-Death Phenotype Is Real and Named — Bileaflet Myxomatous Disease, Inferior Repolarization Changes, Papillary-Muscle Fibrosis, Complex Arrhythmias Without Significant Regurgitation; the Unmasking Column: In Asymptomatic Severe Aortic Stenosis, 44% Show a Normal Resting Filling Pressure but Only 4% Stay Under 25 mmHg Once the Bike Starts, and in Asymptomatic Severe Mitral Regurgitation Exercise Revealed a Systolic Pulmonary Pressure Above 60 mmHg in 34%; the Plumbing Column: Invasive Exercise Testing — Aortic Stenosis Raises Cardiac Output the Least of Any Group, 5.3→12.4 L/min, While the Wedge Pressure Nearly Triples, 11.8→31.4 mmHg; the Training-as-Medicine Column: a Randomized 4-Week Whole-Body-Vibration Program in Severe-AS Patients Awaiting a New Valve Bought +9.6 W of Peak Power Difference With Zero Serious Adverse Events, and 12 Weeks of Prescribed Cardiac Rehabilitation After the Replacement Raised Anaerobic Threshold, VO₂, 6-Minute Walk, Ejection Fraction and Quality of Life; the Comeback-Honesty Column: One Year After Valve Replacement, a Third of Patients Still Carry Elevated Exercise Filling Pressures — the Valve Is Fixed, the Ramp Is Still Earned; the Aorta Fence: Mild Root Enlargement Can Be a Normal Athlete Adaptation, but High-Intensity Work on an Aortopathy Substrate Is the Dissection Trigger; the Scale File: 33.4 Million People Carry Rheumatic Valve Disease Worldwide and Brazil's PROVAR Found It in 42 of Every 1,000 Schoolchildren) — the Answer Is a Triage, Not a Verdict: the Innocent Murmur Is a Full License, the Valve Diagnosis Is a Graded One, Symptom Truth Is Discovered at the Intensities Training Actually Uses, and on the Surgical Road the Training Itself Is Part of the Treatment

By RightRep AI Assistant · · 21 min read

A heart murmur is the door where the internet's two default scripts — the fear script: a murmur means your heart can't take strain, so no lifting, no hard cardio, rest is safety and the dismissive script: everyone has a murmur, it's nothing, train through whatever you feel — both fail the reader at the exact door she walked in through, because this reader is one of three people: the one who heard a sentence at a routine exam — "you have a heart murmur" — and left with no idea what it is; the one holding an echo report that says mitral valve prolapse and a browser full of sudden-death stories; or the Brazilian reader whose murmur traces back to a childhood sore throat that became rheumatic fever, who was told at 20 what her valves look like at 40. The fear script fails because most murmurs are innocent and most valve findings in the community are mild: mitral valve prolapse runs at 2–3% of the general population [1], and when Framingham put 3,491 ordinary people under the echo probe, the MVP they found was "far more benign" than the referral series the fear literature was written from — severe regurgitation in only 6.5% of classic MVP [2]. The dismissive script fails because the tail is real and because "fine at rest" is not "fine under load": in asymptomatic severe aortic stenosis, 44% of patients showed a normal resting filling pressure, but once the exercise bike started, only 4% stayed under 25 mmHg [5], and in asymptomatic severe mitral regurgitation, exercise testing unmasked a systolic pulmonary pressure above 60 mmHg in 34% of those with clean resting numbers [4]. So the fences come first. First: the undifferentiated-murmur fence — a murmur never diagnoses itself; if it is new, or comes with exertional chest pain, fainting or near-fainting, breathlessness out of proportion to the work, new irregular racing palpitations, or a family history of sudden death or aortic disease, that is a cardiology appointment before the next session, not a deload [1][5]. Second: the severity fence — a diagnosed severe aortic stenosis without a cardiology plan means no self-administered maximum-effort testing of any kind; the fences live until the plan exists [3][5]. Third: the aorta fence — a dilated aorta, a bicuspid valve with aortopathy, or Marfan-features body habitus rewrites the rules: intensity caps and no maximal Valsalva on heavy lifts, because high-intensity work on that substrate is the dissection trigger [9]. Fourth: the rheumatic fence — the reader whose valves carry rheumatic scars is on a secondary-prevention contract: the strep throat gets treated, not trained through, and the prophylaxis is never self-edited [10][11]. With the fences standing, the file underneath is one of the strongest inversions in this library's cardiac wing: a murmur is a sound, not a verdict — the innocent murmur is a full license, the valve diagnosis is a graded one, and on the surgical road the training itself is part of the treatment [2][7][8].

The short answer: yes — it's a triage, not a verdict

Strip the file to its spine. The sound: a murmur is turbulence the stethoscope hears — sometimes a normal valve moving a normal volume fast (the innocent murmur of thin chests, pregnancy and high-output fitness), sometimes the signature of a valve that leaks or narrows [1][2]. The community column: MVP, the diagnosis most murmur readers carry, is 2–3% prevalent [1]; in Framingham's 3,491, classic MVP numbered 46 people, severe MR appeared in only 3 of those 46 (6.5%), and left-atrial enlargement in just 8.7% — a profile "far more benign… than previously reported in hospital- or referral-based series" [2]. The tail column: the arrhythmic-MVP phenotype — usually female, bileaflet myxomatous disease, mid-systolic click, repolarization changes in the inferior leads, complex ventricular arrhythmias, often without significant regurgitation, on a substrate of papillary-muscle and inferobasal fibrosis with mitral annulus disjunction — is real, rare, and the reason the dismissive script dies [1]. The unmasking column: "asymptomatic" is a load-dependent claim — 39 asymptomatic severe-AS patients: normal resting filling pressures in 44% of the LA-dilated half, only 4% still under 25 mmHg during exercise [5]; 57 primary-MR patients: exercise revealed sPAP >60 mmHg in 34% of the asymptomatic-with-normal-resting-values group [4]. The plumbing column: under invasive exercise testing, aortic stenosis raised cardiac output the least of any group — 5.3→12.4 L/min against 5.3→16.0 in healthy controls — while the wedge pressure nearly tripled, 11.8→31.4 mmHg, with the steepest pressure-flow slope in the initial phase of exercise, exactly where a warm-up ends and a work set begins [3]. The training-as-medicine column: 30 severe-AS patients awaiting a new valve randomized to four weeks of whole-body vibration — peak power +5.1 W while controls fell −4.5 W (a 9.6 W difference, P=0.01), zero serious adverse events [7]; 60 post-TAVR patients randomized to 12 weeks of prescribed cardiac rehabilitation — anaerobic threshold, peak VO₂, oxygen pulse, peak power, LVEF and 6-minute walk all significantly up, quality of life significantly better, zero complications on symptom-restricted testing [8]. The comeback-honesty column: one year after valve replacement, 12 of 37 patients (32%) still carried elevated exercise filling pressures — predicted by ischemic disease and diffuse fibrosis, unrelated to preoperative stenosis severity [6]. That is the audit in one paragraph: the sound is a question, echo answers it, the severity and symptom columns set the fences, and inside the fences ordinary progressive training is not just permitted but therapeutic [2][7][8].

What the sound actually is: turbulence, and the two families it comes from

The mechanics in a paragraph: a murmur is the noise blood makes when laminar flow breaks into turbulence — through a valve that doesn't open fully (stenosis), across a valve that leaks back (regurgitation), or simply through a perfectly normal valve moving a large volume quickly in a chest that transmits sound well [1][2]. The first family is the innocent murmur: no structural disease, no hemodynamic consequence, common in thin young bodies, athletes with high stroke volumes, and pregnancy — it needs no fence and no program change. The second family is the valvular murmur, and it lives on a spectrum the echo measures precisely: which valve, how narrow or how leaky, what the chambers have remodeled in response, and what happens to pressures when flow rises [3][4][5]. The reader's job at this door is not to self-diagnose which family she is in — that is the one thing the stethoscope-and-echo chain exists to do — but to know that the two families have opposite training contracts, which is exactly why both internet scripts fail: the fear script fences the innocent reader who needed none, and the dismissive script unfences the valve reader who needed them [1][2][5]. The mitral valve prolapse reader sits instructively between them: her diagnosis is common, usually mild, community-benign — and yet it owns the one named sudden-death phenotype in the mild-valve file, which is why her fence is a cardiology risk-stratification question and not a training-frequency question [1][2].

The community column: Framingham against the referral series

The single most steadying receipt in this file is Framingham's. Older MVP literature was written from hospital and referral series — the sickest subset, selected for complications — and painted MVP as a frequent source of severe regurgitation, enlarged atria and clinical trouble [2]. Freed and colleagues flipped the denominator: all 3,491 Framingham Heart Study subjects screened, 150 with possible MVP by echo, quantitatively classified into classic (46) and nonclassic (37) prolapse [2]. The results: leaflet length, MR degree, and atrial and ventricular sizes were "significantly but mildly increased… with mean values typically within normal range"; average MR jet area was mild (15.1%) in classic MVP and trace (8.9%) in nonclassic; MR was severe in only 3 of 46 (6.5%) subjects with classic MVP; left-atrial volume was increased in only 8.7% of classic and 2.7% of nonclassic MVP [2]. The authors' conclusion is the fear script's obituary: the community profile may "influence the perception of and approach to the outpatient with MVP" [2]. Gym translation for the reader diagnosed last Tuesday: the base rate says your MVP is probably a mild, stable finding compatible with ordinary progressive training — and the probability calculation that matters next (whether your valves carry any of the high-risk features) belongs to a cardiologist with an echo report, not to a comment section [1][2].

The tail column: the arrhythmic-MVP phenotype, named and rare

This library's audits earn their keep by pricing the tail honestly, and the mild-valve file owns one: sudden cardiac death in mitral valve prolapse. The Padua group's state-of-the-art paper is the receipt: despite MVP's 2–3% population prevalence, the true burden of "arrhythmic MVP" remains unknown precisely because it is rare against that denominator — and the clinical profile is characterized well enough to name [1]. The phenotype: "a patient, usually female, with mostly bileaflet myxomatous disease, mid-systolic click, repolarization abnormalities in the inferior leads, and complex ventricular arrhythmias with polymorphic/right bundle branch block morphology, without significant regurgitation" [1]. The substrate, from pathology and cardiac MRI of sudden-death victims and arrhythmic patients: fibrosis of the papillary muscles and inferobasal left-ventricular wall, mitral annulus disjunction, and systolic curling — with premature beats arising from the Purkinje tissue documented as ventricular-fibrillation triggers, mechanically stretched into firing by the prolapsing apparatus itself [1]. Two honest readings follow. First: this tail is why "it's nothing, train through palpitations" is a script that can kill a specific person — the reader with the full phenotype routes to electrophysiology, not to another week of pushing through [1]. Second: the tail is not the average MVP — it is a named, identifiable high-risk pattern inside a common, mostly benign diagnosis, and the identification (which imaging, which patient) is exactly what the cardiology workup exists to settle [1]. The reader's translation is precise: MVP is not a diagnosis of a fatal condition; it is a diagnosis that carries one specific question — do I have the arrhythmic features? — and that question has an address [1][2].

The unmasking column: "asymptomatic" is a load-dependent claim

The deepest technical insight this door owns is that valve symptoms are discovered at load, not at rest — which is why the cardiology workup for significant valve disease so often includes an exercise test, and why the gym reader's "but I feel fine walking around" is data from the wrong domain [4][5]. The severe-aortic-stenosis receipt: 39 asymptomatic patients with AVA <1 cm² and peak velocity >3.5 m/s, exercise testing with invasive catheters in place; in the 25 patients (64%) with a dilated left atrium, resting wedge pressure was normal (<12 mmHg) in 44% — but during exercise only 4% stayed under 25 mmHg, and left-atrial volume and E/e′ predicted an exercise wedge pressure above 30 mmHg with AUCs of 0.75 and 0.84 [5]. The mitral-regurgitation receipt: among 57 patients with significant primary MR, the symptomatic carried higher filling pressures at rest (14 vs 11 mmHg) and at peak exercise (30 vs 25 mmHg) — but among the asymptomatic with normal resting values, exercise testing revealed a systolic pulmonary pressure above 60 mmHg in 34% [4]. Meanwhile peak VO₂ was normal in both MR groups — effort capacity hides the pressure file until it doesn't [4]. This column kills both scripts at once: the dismissive reader's "I feel fine" was measured at 0 watts, and the fear reader's catastrophizing mistakes a finding that needs a load test for a verdict of frailty — the truth is that the load test is cheap, safe in supervised hands, and writes the actual fence [4][5]. For the diagnosed reader, the practical rule: symptom truth is discovered at the intensities training actually uses, under supervision, before those intensities are used alone [3][4][5].

The plumbing column: why valves are load-sensitive, in numbers

The invasive exercise file explains mechanically why this wing of the library treats valve disease differently from everything else muscular. One hundred sixty-eight subjects over age 50 with preserved ejection fraction — 40 with aortic stenosis, 43 with mitral regurgitation, 52 post-infarction, 33 healthy — exercised with right-heart catheters in place, pressures and output measured at rest, 25 W, 75 W and peak [3]. The numbers that matter to a training week: in aortic stenosis, cardiac output rose the least of any group — 5.3→12.4 L/min, against 5.3→16.0 in the healthy — while the wedge pressure nearly tripled, 11.8→31.4 mmHg, versus 8.3→21.1 in healthy controls [3]. The pressure-flow slope — millimeters of pressure per liter of output — was steepest in the initial phase of the exercise test in every group: the lungs take their pressure hit early, exactly where a warm-up ends and the first work set begins [3]. And the slopes ranked the pathologies: aortic stenosis steepest overall (3.0±1.3 mmHg/L/min), MR intermediate (1.9±1.4), healthy shallowest (1.3±1.1) [3]. Gym translation, stated carefully: a narrowed or leaking valve doesn't just "make exercise harder" in the vague way the internet says — it changes the shape of the response, front-loading the pressure cost of every increment, which is why the valve reader's program respects gradual warm-up ladders, long enough between-set recovery for pressures to settle, and the zone-2 floor before any high-intensity ceilings [3]. It is also why this file's fences are about symptoms under load rather than diagnoses at rest [4][5].

The training-as-medicine column: receipts on both sides of the new valve

The inversion that redeems this whole door: for the valve patient on the surgical road, exercise training is not the risk being managed — it is part of the treatment, with randomized receipts on both sides of valve replacement. Before the new valve: 30 severe-AS patients awaiting TAVI (mean valve area 0.75 cm², mean age 79.7), randomized to four weeks of supervised oscillatory whole-body vibration — 12 sessions of 30 minutes — against usual care: peak VO₂ rose 0.3 mL/min/kg in the training group while controls fell 1.4 (difference 1.7, P=0.03); peak power rose 5.1 W while controls fell 4.5 W (difference 9.6 W, P=0.01); and zero serious adverse events occurred in the training group [7]. The authors frame it against exactly the script this door audits: exercise is "generally discouraged" in severe symptomatic AS over safety concerns — yet dosed, supervised, low-impact training was feasible, safe, and preserved capacity that waiting alone erodes [7]. After the new valve: 60 patients with chronic heart failure post-TAVR randomized to 12 weeks of cardiopulmonary-test-prescribed cardiac rehabilitation versus conventional care — anaerobic threshold, peak oxygen uptake, oxygen pulse, peak power, LVEF and 6-minute-walk distance all significantly higher in the training group, quality-of-life scores significantly better, and every symptom-restricted test completed without complications [8]. Add the honesty file: one year after surgical replacement, 12 of 37 patients (32%) still carried an exercise wedge pressure ≥28 mmHg — predicted by coexisting ischemic disease and diffuse myocardial fibrosis, and unrelated to how severe the stenosis had been before surgery [6]. Together the three receipts write the comeback doctrine: the prosthesis fixes the valve, not necessarily the exercise physiology; the ramp back is earned on a supervised calendar; and the training done before and after is measurably medicine [6][7][8].

The aorta fence: the athlete's aorta and the aortopathy line

One column of this file has nothing to do with the valve leaflets and everything to do with the pipe they sit in. Thoracic aortic dilation is progressive, driven by aging and by pathological substrates — connective-tissue disorders, inflammatory and shear-stress disease, and severe valvular heart disease itself — and it carries the one emergency this wing can produce: dissection [9]. The review's two-sided receipt: mild aortic-root enlargement may be observed in athletes and is considered a normal adaptation to regular exercise training — the athlete's aorta is a real, benign phenomenon — but high-intensity physical activity in individuals with a particular genetic substrate, such as gene variants associated with Marfan syndrome or other inherited aortopathies, can favor excessive aortic enlargement and trigger acute aortic dissection [9]. Hence a fence that is structural, not motivational: the reader with a bicuspid aortic valve, a known dilated aorta, or Marfan-features habitus trains under an aorta contract — intensity capped by the cardiologist's measurements, blood pressure managed, no maximal Valsalva on heavy pulls and squats, and any new chest or back pain is an emergency-room sentence, not a foam-roller one [9]. The distinction matters because the same echo that answers the murmur question measures the aorta in the same beat — which is why this file's triage sends the undifferentiated reader to the imaging chain once, properly, instead of to the internet forever [9].

The rheumatic wing: the Brazilian column, from sore throat to valve

The pt-BR twin of this door exists because the world's valve file is not evenly distributed. Globally, rheumatic heart disease — valves scarred by childhood rheumatic fever after a strep throat — still counted 33.4 million prevalent cases, 319,400 deaths and 10.5 million disability-adjusted life-years in 2015, with age-standardized mortality down 47.8% since 1990 but the burden concentrated in the poorest regions [10]. Brazil's receipt is PROVAR: 5,996 schoolchildren screened across 21 public schools in Minas Gerais — rheumatic heart disease in 42 per 1,000 (37 borderline + 5 definite per 1,000), with pathologic mitral regurgitation in 80.9% and aortic regurgitation in 15.1% of the affected, higher prevalence in girls (48 vs 35 per 1,000, P=0.016) and in older children [11]. The regional file confirms the pattern: across Latin America and the Caribbean, prevalence in schoolchildren runs 0.24–48 per 1,000, the literature is "mainly from Brazil", and three established echo-screening programs exist in the region [12]. Two columns follow for the training reader. First, the prevention contract: rheumatic valve disease begins as a strep throat — the sick-day door's rule (fever and throat get rest and treatment, not sessions) is, in this wing, a cardiac-prevention rule decades downstream, and the reader already carrying rheumatic scars is on a secondary-prophylaxis contract that is never self-edited [10][11]. Second, the training license itself: a rheumatic valve is still a valve diagnosis — graded by the same severity brackets, fenced by the same symptom-truth columns, and trainable inside those fences like any other [3][4][5].

The program in gym terms: what stops, what ramps, what never changes

Stops and refers, today: a new murmur with exertional chest pain, fainting or near-fainting, breathlessness out of proportion, new irregular racing palpitations, or a family history of sudden death or aortic disease — cardiology before the next session [1][5]; any new chest or back pain in the dilated-aorta reader — the emergency department, now [9].

Ramps on supervision, not on feelings: the diagnosed valve reader earns intensity through the supervised exercise test that writes her actual brackets [4][5]; the post-replacement reader ramps on the rehabilitation calendar — a third of patients still carry elevated exercise filling pressures a year after the valve was fixed [6], and the 12-week prescribed programs are the receipts that the ramp pays [7][8].

Doses the warm-up as medicine, not ritual: the pressure-flow slope is steepest in the first phase of exercise [3] — the warm-up ladder is where the valve reader spends her caution budget, and zone-2 volume is the base of the pyramid before any ceiling exists.

Never changes: the overload principle (graded, patient, honest), honest tracking of what each session actually felt like — the rep score and form check exist so effort is measured, not guessed — set structure with rest timers long enough for pressures to settle, tempo controlled rather than ballistic, symmetry kept honest; the strep-throat and prophylaxis contract for the rheumatic reader [10][11]; and the wider cardiac wing's doors — heart attack, atrial fibrillation, heart failure, blood pressure — for the readers whose file crosses over, and prevention for the readers building the habit at 40-plus.

The bottom line

  • The triage: a murmur is a sound, not a diagnosis — innocent murmurs are full licenses; valve findings are graded licenses fenced by severity and symptom-truth, and the grading belongs to echo, not to self-diagnosis [1][2][5].
  • The community column: MVP is 2–3% prevalent [1]; Framingham 3,491 — severe MR in only 6.5% of classic MVP, LA enlargement in 8.7%, profile "far more benign" than referral series [2].
  • The tail column: arrhythmic MVP is a named phenotype — bileaflet myxomatous disease, inferior repolarization changes, papillary-muscle/inferobasal fibrosis, annulus disjunction, complex arrhythmias often without significant regurgitation — rare, real, and it routes to electrophysiology, not to a deload [1].
  • The unmasking column: asymptomatic severe AS — 44% normal at rest, only 4% under 25 mmHg on the bike [5]; asymptomatic severe MR — exercise sPAP >60 mmHg in 34% of those with clean resting values [4].
  • The plumbing column: invasive exercise testing — AS raised cardiac output least (5.3→12.4 vs 5.3→16.0 L/min in healthy) while the wedge pressure nearly tripled (11.8→31.4 mmHg), slope steepest in the initial phase [3].
  • The training-as-medicine column: pre-TAVI whole-body vibration — peak power +9.6 W difference, zero serious adverse events [7]; post-TAVR cardiac rehabilitation — AT, VO₂, oxygen pulse, peak power, LVEF, 6MWD and QoL all significantly better, zero complications [8].
  • The comeback-honesty column: 32% of AVR patients still exercise-elevated at one year — predicted by ischemia and fibrosis, not preoperative severity; the ramp is earned [6].
  • The aorta fence: mild root enlargement can be normal athlete adaptation, but high intensity on an aortopathy substrate is the dissection trigger — intensity caps, no maximal Valsalva [9].
  • The scale file: 33.4M RHD cases and 319,400 deaths worldwide in 2015 [10]; Brazil PROVAR — 42/1,000 schoolchildren, mitral 80.9% of the affected [11]; LatAm schoolchildren 0.24–48/1,000, the literature mainly Brazilian [12].
  • The honest nulls: the arrhythmic-MVP burden is explicitly unknown against its denominator [1]; peak VO₂ was normal in both MR symptom groups — capacity hides the pressure file [4]; and no column in this file fences the innocent murmur [2].

Train like the file reads: get the sound named once, respect the fences it earns, and let the camera count the reps of the long game at rightrep.app.

This post was written by the RightRep AI Assistant — the same AI that counts and scores your reps at rightrep.app.

Sources

  1. Basso C, Iliceto S, Thiene G, Perazzolo Marra M. Mitral Valve Prolapse, Ventricular Arrhythmias, and Sudden Death. Circulation, 2019;140(11):952–964. pubmed.ncbi.nlm.nih.gov
  2. Freed LA, Benjamin EJ, Levy D, et al. Mitral valve prolapse in the general population: the benign nature of echocardiographic features in the Framingham Heart Study. Journal of the American College of Cardiology, 2002;40(7):1298–1304. pubmed.ncbi.nlm.nih.gov
  3. Andersen MJ, Wolsk E, Bakkestrøm R, et al. Pressure-flow responses to exercise in aortic stenosis, mitral regurgitation and diastolic dysfunction. Heart, 2022;108(23):1895–1903. pubmed.ncbi.nlm.nih.gov
  4. Bakkestrøm R, Banke A, Christensen NL, et al. Hemodynamic Characteristics in Significant Symptomatic and Asymptomatic Primary Mitral Valve Regurgitation at Rest and During Exercise. Circulation: Cardiovascular Imaging, 2018;11(2):e007171. pubmed.ncbi.nlm.nih.gov
  5. Christensen NL, et al. Association Between Left Atrial Dilatation and Invasive Hemodynamics at Rest and During Exercise in Asymptomatic Aortic Stenosis. Circulation: Cardiovascular Imaging, 2016;9(10):e005156. pubmed.ncbi.nlm.nih.gov
  6. Carter-Storch R, Dahl JS, Christensen NL, et al. Exercise Hemodynamics After Aortic Valve Replacement for Severe Aortic Stenosis. Journal of the American Society of Echocardiography, 2018;31(10):1091–1100. pubmed.ncbi.nlm.nih.gov
  7. Klaus J, Gerhardt F, Nienaber S, et al. Safety and effectiveness of oscillatory whole-body vibration training on exercise capacity and physical performance in aortic valve stenosis patients prior to transcatheter aortic valve implantation: a randomized clinical trial. Clinical Research in Cardiology, 2025 (online ahead of print). pubmed.ncbi.nlm.nih.gov
  8. Song J, Chen X, Wang B, Cheng X, Wang Y. Effect of Exercise-Based Cardiac Rehabilitation on Patients With Chronic Heart Failure After Transcatheter Aortic Valve Replacement: A Randomized Controlled Trial. Journal of Cardiopulmonary Rehabilitation and Prevention, 2025;45(1):51–56. pubmed.ncbi.nlm.nih.gov
  9. Monda E, Verrillo F, Rubino M, et al. Thoracic Aortic Dilation: Implications for Physical Activity and Sport Participation. Diagnostics, 2022;12(6):1392. pubmed.ncbi.nlm.nih.gov
  10. Watkins DA, Johnson CO, Colquhoun SM, et al. Global, Regional, and National Burden of Rheumatic Heart Disease, 1990–2015. New England Journal of Medicine, 2017;377(8):713–722. pubmed.ncbi.nlm.nih.gov
  11. Nascimento BR, Beaton AZ, Nunes MC, et al. Echocardiographic prevalence of rheumatic heart disease in Brazilian schoolchildren: Data from the PROVAR study. International Journal of Cardiology, 2016;219:439–445. pubmed.ncbi.nlm.nih.gov
  12. Jaimes-Reyes MA, Urina-Jassir M, Urina-Triana M, et al. Current Situation of Acute Rheumatic Fever and Rheumatic Heart Disease in Latin America and the Caribbean: A Systematic Review. Global Heart, 2022;17(1):65. pubmed.ncbi.nlm.nih.gov