Left Ventricular Hypertrophy — DVA claim example

Diagnostic Assessment — Left Ventricular Hypertrophy

Example 1 of 1 · fictitious patient (Veteran CA)

Diagnostic Assessment

Left Ventricular Hypertrophy

No Statement of Principles applies to this condition (non-SOP claim).

ADF History

Veteran CA, date of birth 14 June 1972, Australian Army, Rifleman (Infantry), later Small Arms Coach and Range Instructor, enlisted 08 January 1990, medically discharged 30 June 2014. Operational service: Somalia, 12 January 1993 to 21 May 1993 (warlike); East Timor, 20 September 1999 to 20 February 2000 (warlike); Afghanistan, 05 September 2007 to 15 April 2008 (warlike).

Occupational History

As an infantry soldier the veteran conducted patrols, field exercises and live-fire training carrying heavy loads, with irregular meals and sleep. From 1998 he worked as a small arms coach and range instructor, spending most working days on indoor and outdoor firing ranges where lead-based ammunition generates airborne lead fume and dust, and where lead contamination of hands, food and clothing is common. Range instructors in this period undertook regular blood lead surveillance because of this recognised hazard.

On operations infantry soldiers are exposed to traumatic events, sustained stress and disrupted sleep, and deployed members commonly have limited access to their regular medications and medical devices. The service culture of the period normalised heavy drinking after exercises and on return from deployment, and gym-based strength training on bases, sometimes with unregulated supplements and anabolic agents, was widespread.

History

Veteran CA, an infantry soldier and range instructor in the Australian Army, developed left ventricular hypertrophy on 12 May 2008, shortly after warlike service in Afghanistan, on a background of hypertension, chronic kidney disease, obesity, obstructive sleep apnoea, type 2 diabetes, heavy alcohol use linked to posttraumatic stress disorder, elevated blood lead from range duties and anabolic steroid use on deployment. The condition was confirmed on echocardiography on 15 August 2008 and worsened in 2012 with uncontrolled hypertension and untreated sleep apnoea.

Timeline

• 22 Mar 2005 — At a garrison health centre the medical officer diagnosed essential hypertension, with clinic blood pressures averaging 162/104 mmHg confirmed on ambulatory monitoring. Weight was 112 kg and BMI 33.4, up from 88 kg in 1999. Alcohol intake was recorded at eight to ten standard drinks a day since his return from East Timor in 2000. Perindopril was commenced. Posttraumatic stress disorder from Somalia and East Timor had been diagnosed by a psychiatrist in 2004. "hypertension, BP 162/104, BMI 33.4"
• 14 Feb 2006 — Routine lead surveillance for range staff showed a blood lead of 1.8 micromol/L. Repeat levels remained between 1.2 and 1.9 micromol/L through 2006 and 2007 despite range ventilation changes. In the same year serum creatinine was raised with an eGFR of 52 mL/min/1.73 m2, persisting on repeat testing, and chronic kidney disease stage 3a was diagnosed, attributed to years of daily anti-inflammatory use for a service back injury and to hypertension. "blood lead 1.8, eGFR 52"
• 19 Sep 2006 — Polysomnography showed moderate obstructive sleep apnoea, with an apnoea-hypopnoea index of 34 events per hour and desaturation to 82 per cent. CPAP was commenced with a good response. In March 2007 an HbA1c of 7.4 per cent confirmed type 2 diabetes mellitus and metformin was started. "OSA AHI 34, CPAP started"
• 10 Aug 2007 — Pre-deployment medical examination recorded blood pressure 138/88 mmHg on perindopril. The resting ECG showed sinus rhythm without left ventricular hypertrophy voltage criteria or repolarisation changes. He passed his basic fitness assessment. "ECG normal, no LVH"
• 10 Mar 2008 — On warlike service in Afghanistan the medical officer recorded a blood pressure of 168/106 mmHg at a sick parade for headaches. The veteran's perindopril had run out in December 2007 and resupply had not arrived, and he had not used CPAP since arriving because the machine would not run on the deployed power supply. He reported training heavily in the base gym. "BP 168/106, no perindopril"
• 20 May 2008 — At his post-deployment health assessment he reported exertional breathlessness and palpitations since failing a run on 12 May 2008. Blood pressure was 174/108 mmHg. In Afghanistan his perindopril supply had run out for about four months and his CPAP machine had not worked on the deployed power supply. He disclosed injecting nandrolone and testosterone obtained at the base gym from October 2007 to April 2008. Haematocrit was 0.55. The ECG showed left ventricular hypertrophy by Sokolow-Lyon voltage criteria with lateral strain pattern. "LVH on ECG, steroids disclosed"
• 15 Aug 2008 — Transthoracic echocardiography showed concentric left ventricular hypertrophy, with an interventricular septum of 14 mm, posterior wall of 13 mm and left ventricular mass index of 142 g/m2, normal ejection fraction and grade 1 diastolic dysfunction. A cardiologist diagnosed hypertensive left ventricular hypertrophy with contributions from anabolic steroid use, obesity, sleep apnoea, renal impairment and alcohol. Amlodipine was added and steroid cessation and alcohol reduction advised. "concentric LVH, LVMI 142"
• 30 Mar 2012 — His CPAP machine failed in March 2012 and a replacement was not supplied for nine months. Ambulatory blood pressure monitoring showed a mean daytime pressure of 168/104 mmHg despite two agents, and he was still drinking about 80 grams of alcohol a day. A referral for cardiology review was placed on a waiting list. "CPAP failed, ABPM 168/104"
• 12 Nov 2012 — Repeat echocardiography showed progression of the left ventricular hypertrophy, with an interventricular septum of 17 mm, left ventricular mass index of 168 g/m2, grade 2 diastolic dysfunction and left atrial enlargement. He reported breathlessness on climbing one flight of stairs. The cardiologist recorded clear worsening of the left ventricular hypertrophy. "LVMI 168, grade 2 diastolic"

Symptoms

At onset the veteran had breathlessness and palpitations on exertion and could no longer complete his fitness assessment run. After onset he developed fatigue, reduced exercise tolerance and episodes of chest tightness on heavy exertion.

He now reports breathlessness on climbing one flight of stairs or walking uphill, palpitations, ankle swelling at the end of the day and fatigue. He has been told he has diastolic heart failure and takes three antihypertensive medications.

He has had to give up running and heavy lifting, and he becomes breathless carrying shopping up stairs. He reports that the breathlessness worsened noticeably after 2012.

Imaging

• 10 Aug 2007 — Resting 12-lead ECG: "Sinus rhythm. No left ventricular hypertrophy voltage criteria. No repolarisation abnormality."
• 20 May 2008 — Resting 12-lead ECG: "Sinus rhythm. Sokolow-Lyon voltage 42 mm, meeting criteria for left ventricular hypertrophy, with lateral ST depression and T-wave inversion (strain pattern)."
• 15 Aug 2008 — Transthoracic echocardiogram: "Concentric left ventricular hypertrophy: septum 14 mm, posterior wall 13 mm, LV mass index 142 g/m2. LVEF 62 per cent. Grade 1 diastolic dysfunction. Normal aortic valve."
• 12 Nov 2012 — Transthoracic echocardiogram: "Progressive concentric left ventricular hypertrophy: septum 17 mm, posterior wall 15 mm, LV mass index 168 g/m2. LVEF 58 per cent. Grade 2 diastolic dysfunction. Left atrial volume index 41 mL/m2."

Onset Date

The most likely date of onset of this condition is 12 May 2008.

At that date the veteran was serving full time with an infantry training establishment in Australia, four weeks after returning from warlike service in Afghanistan on 15 April 2008. He had hypertension that had been uncontrolled for months on deployment, chronic kidney disease, obesity, obstructive sleep apnoea untreated on deployment, type 2 diabetes and an elevated blood lead, was drinking heavily, and had stopped anabolic steroids two to three weeks earlier.

This date is appropriate because his pre-deployment ECG of 10 August 2007 showed no left ventricular hypertrophy and he passed his fitness assessment, while on 12 May 2008 he first became breathless and failed a run, and the ECG of 20 May 2008 showed left ventricular hypertrophy with strain, confirmed on echocardiography on 15 August 2008. It falls within uninterrupted full-time service.

For the hypertension cause, the 2 years before onset run from 12 May 2006 to 12 May 2008, and hypertension was diagnosed on 22 Mar 2005. For the obesity and alcohol causes, the 5 years before onset run from 12 May 2003 to 12 May 2008; his BMI exceeded 30 from 2002 and his alcohol intake averaged about 80 grams a day over that period. For the anabolic steroid cause, the 2 years before onset run from 12 May 2006 to 12 May 2008, and he used nandrolone and testosterone for seven months, from October 2007 to April 2008. For the lead cause, the 12 months before onset run from 12 May 2007 to 12 May 2008, during which his blood lead remained above 1.0 micromol/L. Chronic kidney disease, obstructive sleep apnoea and type 2 diabetes were each established before 12 May 2008 and present on that date.

For the worsening causes, the documented worsening was on 12 Nov 2012. The 6 months before the worsening run from 12 May 2012 to 12 Nov 2012, during which his blood pressure remained uncontrolled at a mean of 168/104 mmHg, he drank about 80 grams of alcohol a day, and his sleep apnoea went untreated after his CPAP machine failed in March 2012.

1. What is the formal diagnosis of the condition claimed above?

The formal diagnosis is Left Ventricular Hypertrophy (ICD-10-AM I51.7), concentric in pattern, with diastolic dysfunction. No Statement of Principles has been determined for left ventricular hypertrophy.

Left ventricular hypertrophy is a pathological thickening of the wall of the left ventricle, the main pumping chamber of the heart, usually in response to chronic pressure or volume overload. It develops most often from long-standing high blood pressure, and is promoted by obesity, sleep apnoea, chronic kidney disease, diabetes, alcohol excess and anabolic steroids. The thickened muscle becomes stiff, impairing filling of the heart, and is an independent risk factor for heart failure, atrial fibrillation, ischaemic heart disease, ventricular arrhythmias, stroke and sudden death.

The diagnosis followed years of hypertension, obesity, sleep apnoea, renal impairment and heavy drinking, with lead exposure from range duties and anabolic steroid use and interrupted treatment on deployment. It began on 12 May 2008, was confirmed on echocardiography on 15 August 2008 and worsened in 2012.

The pattern in this veteran is concentric hypertrophy with diastolic dysfunction, typical of pressure overload from hypertension, compounded by anabolic steroids, obesity, sleep apnoea and renal impairment. A normal aortic valve excluded aortic stenosis, and there was no family history or echocardiographic pattern suggesting hypertrophic cardiomyopathy.

2. For each diagnosis identified, please also provide the following dates:

When did the veteran first experience symptoms attributable to this condition?

12 May 2008.

When did the veteran first present to a health / medical provider for this condition?

20 May 2008.

When was the condition confirmed / formally diagnosed?

15 August 2008.

When did the veteran first present to you (or your practice) for this condition?

04 February 2025.

3. How was this diagnosis confirmed? i.e. what were the key symptoms and signs, investigation results, specialist opinions?

The diagnosis was confirmed by transthoracic echocardiography on 15 August 2008, which showed concentric left ventricular hypertrophy with an interventricular septum of 14 mm, a posterior wall of 13 mm and a left ventricular mass index of 142 g/m2, above the upper limit of normal of 115 g/m2 for men, with preserved ejection fraction and grade 1 diastolic dysfunction. The aortic valve was normal, excluding aortic stenosis as the cause.

The ECG of 20 May 2008 met Sokolow-Lyon voltage criteria with a strain pattern, compared with a normal ECG on 10 August 2007. A cardiologist confirmed the diagnosis. Repeat echocardiography on 12 November 2012 confirmed progression, with a septum of 17 mm, a left ventricular mass index of 168 g/m2 and grade 2 diastolic dysfunction.

4. What do you consider to be the cause(s) of the condition in this veteran? Give consideration to constitutional and common risk factors, pre-existing injuries or diseases, and occupational or lifestyle risks, as well as direct causative mechanisms.

No Statement of Principles has been determined for left ventricular hypertrophy. The claim is therefore decided on the sound medical-scientific evidence of what causes the condition, without the limits a Statement of Principles would impose, and the recognised causes below are drawn from the cardiology literature.

Legislation: the clinical onset of this condition was on 12 May 2008, after 1 July 2004, during continuous full-time service. This is a Military Rehabilitation and Compensation Act 2004 (MRCA) claim. The reasonable hypothesis standard applies to his warlike service in Somalia in 1993, East Timor in 1999 to 2000 and Afghanistan in 2007 to 2008, where his posttraumatic stress disorder and drinking arose, his treatment was interrupted and he used anabolic steroids, and the balance of probabilities standard applies to his peacetime service, including his range duties and the 2012 worsening. Each cause must be related to service. Under the beneficial approach required by the legislation, the absence of documentation does not mean that an event or exposure did not occur: lack of evidence is not evidence of lack.

Recognised causes on the medical-scientific evidence (no Statement of Principles)

Causative factors

Cause 1: having hypertension for at least the 2 years before the clinical onset of left ventricular hypertrophy; — MET

- Essential hypertension was diagnosed on 22 March 2005, with a mean blood pressure of 162/104 mmHg on ambulatory monitoring, and was present throughout the 2 years before onset, from 12 May 2006 to 12 May 2008. On warlike service in Afghanistan his perindopril supply ran out for about four months, and his blood pressure was 174/108 mmHg on 20 May 2008. The hypertension was driven by service-related heavy drinking, obesity and sleep apnoea. Chronic pressure overload is the leading cause of left ventricular hypertrophy.

Cause 2: having chronic kidney disease, with an estimated glomerular filtration rate of less than 60 mL/min/1.73 m2 for at least 3 months, at the time of the clinical onset of left ventricular hypertrophy; — MET

- Chronic kidney disease stage 3a was diagnosed in 2006, with an eGFR of 52 mL/min/1.73 m2 persisting on repeat testing, attributed to years of daily anti-inflammatory use prescribed for a service back injury and to hypertension. It was present at onset on 12 May 2008. Renal impairment causes volume and pressure overload and promotes myocardial hypertrophy and fibrosis.

Cause 3: being obese, with a body mass index of 30 or more, for at least the 5 years before the clinical onset of left ventricular hypertrophy; — MET

- The veteran's weight rose from 88 kg in 1999 to 112 kg by 2005, BMI 33.4, after a service knee injury restricted his activity and with heavy drinking. His BMI exceeded 30 from 2002 throughout the 5 years before onset, from 12 May 2003 to 12 May 2008. Obesity increases cardiac output and blood volume and independently increases left ventricular mass.

Cause 4: having obstructive sleep apnoea at the time of the clinical onset of left ventricular hypertrophy; — MET

- Moderate obstructive sleep apnoea was confirmed on polysomnography on 19 September 2006, with an apnoea-hypopnoea index of 34. On warlike service in Afghanistan from September 2007 to April 2008 his CPAP machine would not run on the deployed power supply and the apnoea went untreated. It was present at onset on 12 May 2008. Repeated nocturnal hypoxia and surges in blood pressure promote left ventricular hypertrophy.

Cause 5: having diabetes mellitus at the time of the clinical onset of left ventricular hypertrophy; — MET

- Type 2 diabetes mellitus was diagnosed in March 2007 with an HbA1c of 7.4 per cent, on a background of service-related obesity, and was present at onset on 12 May 2008. Diabetes causes insulin-mediated myocardial growth and fibrosis independent of blood pressure.

Cause 6: consuming an average of at least 60 grams of alcohol per day for at least the 5 years before the clinical onset of left ventricular hypertrophy; — MET

- After his return from warlike service in East Timor in February 2000 the veteran drank eight to ten standard drinks a day, recorded on 22 March 2005, as part of the posttraumatic stress disorder arising from Somalia and East Timor diagnosed in 2004. His average intake of about 80 grams a day continued throughout the 5 years before onset, from 12 May 2003 to 12 May 2008, apart from reduced drinking on deployment. Heavy alcohol use raises blood pressure and is directly toxic to the myocardium.

Cause 7: using anabolic-androgenic steroids for a cumulative period of at least 6 months within the 2 years before the clinical onset of left ventricular hypertrophy; — MET

- On warlike service in Afghanistan the veteran injected nandrolone and testosterone obtained through the base gym from October 2007 to April 2008, about seven months, disclosed on 20 May 2008 with a haematocrit of 0.55. This fell within the 2 years before onset, from 12 May 2006 to 12 May 2008. Anabolic-androgenic steroids cause pathological concentric hypertrophy, raise blood pressure and impair diastolic function.

Cause 8: having a blood lead level of at least 1.0 micromol/L for at least the 12 months before the clinical onset of left ventricular hypertrophy; — MET

- As a range instructor on indoor and outdoor firing ranges from 1998, including range practices conducted on deployment, the veteran had blood lead levels between 1.2 and 1.9 micromol/L on routine surveillance from 14 February 2006 to April 2008. This covered the 12 months before onset, from 12 May 2007 to 12 May 2008. Chronic lead exposure raises blood pressure and is associated with increased left ventricular mass.

Worsening factors

Worsening 1: having uncontrolled hypertension, with a mean blood pressure of at least 140/90 mmHg, for at least the 6 months before the clinical worsening of left ventricular hypertrophy; — MET

- Ambulatory monitoring on 30 March 2012 showed a mean daytime blood pressure of 168/104 mmHg despite two agents, and clinic readings remained above 160/100 mmHg throughout the 6 months before the worsening, from 12 May 2012 to 12 November 2012.

Worsening 2: consuming an average of at least 60 grams of alcohol per day for at least the 6 months before the clinical worsening of left ventricular hypertrophy; — MET

- The veteran's drinking, linked to his service-related posttraumatic stress disorder, continued at about 80 grams a day throughout the 6 months before the worsening, from 12 May 2012 to 12 November 2012.

Worsening 3: having untreated obstructive sleep apnoea at the time of the clinical worsening of left ventricular hypertrophy; — MET

- His CPAP machine failed in March 2012 and a replacement was not supplied for nine months, so his moderate obstructive sleep apnoea was untreated at the documented worsening on 12 November 2012.

Worsening 4: inability to obtain appropriate clinical management for left ventricular hypertrophy. — MET

- On warlike service in Afghanistan in 2007 to 2008 his antihypertensive supply ran out for about four months and his CPAP could not be used. In 2012 his failed CPAP machine was not replaced for nine months and his cardiology referral sat on a waiting list while his blood pressure was uncontrolled. The left ventricular mass index rose from 142 to 168 g/m2. Under Brew v Repatriation Commission (1999) this is an inability to obtain appropriate clinical management.

The % contribution of the causes is 100% and significant.

Sequelae

The left ventricular hypertrophy is a sequela of the veteran's accepted conditions: hypertension, obstructive sleep apnoea, chronic kidney disease, obesity and the alcohol use disorder that accompanies his posttraumatic stress disorder. The left ventricular hypertrophy has in turn led to diastolic dysfunction with heart failure with preserved ejection fraction and left atrial enlargement, increasing his risk of atrial fibrillation.

Unintended Consequence

Met. The chronic kidney disease contributing to the left ventricular hypertrophy is in part an unintended consequence of long-term anti-inflammatory medication prescribed by Defence medical officers for his service back injury (section 6A of the DRCA and the equivalent provisions of the MRCA).

Inability to Attain Appropriate Medical Management

MET. On warlike service in Afghanistan from September 2007 to April 2008 his perindopril ran out for about four months and his CPAP machine could not run on deployed power, so his hypertension and sleep apnoea went untreated in the months before onset. In 2012 his failed CPAP machine was not replaced for nine months and his cardiology referral was delayed while his blood pressure remained uncontrolled, and the left ventricular mass index rose from 142 to 168 g/m2. Applying the objective and subjective tests in Brew v Repatriation Commission (Full Federal Court, 10 September 1999, Merkel J), interruption of prescribed treatment by operational constraints and delays in supplying essential devices and specialist review amount to an inability to obtain appropriate clinical management.

5. Please provide a Health Summary and a medication / prescribing history.

See attached report.

References

1. 2004, Psychiatric assessment, Consultant psychiatrist
2. 22 Mar 2005, Outpatient health record and ambulatory blood pressure report, Medical Officer, Garrison health centre
3. 14 Feb 2006, Blood lead surveillance results, Occupational health service
4. 2006, Renal function tests and specialist letter, Renal physician
5. 19 Sep 2006, Diagnostic polysomnography report, Sleep physician
6. Mar 2007, Pathology report, HbA1c, Medical Officer
7. 10 Aug 2007, Pre-deployment medical examination and ECG, Medical Officer
8. 10 Mar 2008, Deployed health record, Medical Officer, Afghanistan
9. 20 May 2008, Post-deployment health assessment and ECG, Medical Officer
10. 15 Aug 2008, Echocardiogram and cardiology consultation, Cardiologist
11. 30 Mar 2012, Ambulatory blood pressure report, Medical Officer
12. 12 Nov 2012, Repeat echocardiogram and cardiology review, Cardiologist