chapter 25 Cardiology
INTRODUCTION AND OVERVIEW
Cardiovascular disorders are encountered very frequently in the primary care setting. In developed or affluent countries, cardiovascular disease is still the most common cause of mortality, accounting for 38% of all deaths,1 and a significant cause of disability, particularly due to cerebrovascular disease and congestive cardiac failure. One in five Australians are affected by cardiovascular disease.2 Cardiovascular disorders are due to pathologies that arise in the:
THE INTEGRATIVE APPROACH IN CARDIOLOGY
In 2005 the American College of Cardiology published an expert consensus document titled, ‘Integrating complementary medicine into cardiovascular medicine’.3 The authors noted that there was considerable debate regarding the clinical utility of alternative medicine practices, that these practices were widely employed by patients with cardiovascular disease and that there was a need for further research. The authors noted that ‘integrating CAM into medicine must be guided by compassion, but enhanced by science and made meaningful through solid doctor/patient relationships. Most importantly CAM involves a commitment from the clinician to the caring of patients on a physical, mental and spiritual level’.3a
ASSESSMENT OF THE CARDIOVASCULAR SYSTEM
CARDIOVASCULAR HISTORY
• Chest pain—ask about the onset, character, duration, severity (on a scale of 1 to 10, with 10 being the most severe pain the patient has ever experienced), radiation, relieving and exacerbating factors, associated other symptoms (e.g. nausea, vomiting, diaphoresis). If it is effort angina, ask how far the patient can walk before experiencing angina (‘angina distance’). Although chest pain of cardiac origin is often of the textbook type (e.g. severe, central, crushing, radiating to the neck and/or left arm, associated with sweating and nausea), it is also often atypical, especially in women, the elderly and diabetics. Therefore atypical chest pain is often misdiagnosed in these groups and a surprising number of heart attacks are ‘silent’ or go unrecognised.
• Dyspnoea—ask about the onset, duration, progression, relationship to rest or exertion, any associated orthopnoea, paroxysmal nocturnal dyspnoea, level of effort tolerance (how far the patient can walk before feeling breathless—‘dyspnoea distance’).
• Palpitations—ask about the onset, frequency, duration, trigger factors (e.g. caffeine, smoking, anxiety), pattern (ask the patient to tap on a table to demonstrate the rhythm they felt), associated symptoms (presyncope), relieving factors.
• Syncope—ask about any premonitions, what the patient was doing at the time of onset, any postural changes, any associated vertigo (a feature that would favour a neurological association), incontinence, any similar previous episodes, post-event drowsiness (may weigh in favour of an ictal episode) and account of a bystander witness.
• Ask about intercurrent illnesses and past history of other illnesses. Associated kidney disease, endocrine disorders, stroke or peripheral vascular disease has relevance to the cardiovascular system.
• Ask about the risk factors for cardiovascular disease, particularly coronary artery disease (see later section on risk factors). Obtain details about family history of cardiac disease.
• Obtain a detailed medication history, paying particular attention to cardiovascular medications and agents that can affect the cardiovascular system. Always ask about allergies.
• Family history is of significant importance in the cardiac history. Do not forget to probe into the social history, focusing on occupational status, cigarette smoking, alcohol and substance consumption/abuse, dietary habits, recreational physical activity and travels.
• Ask about stress and mental health issues. Ischaemic chest pain is commonly precipitated in response to an acute stressor, and major acute stressors and panic attacks are risk factors for precipitating cardiac events. Poor long-term mental health is also an independent risk factor for cardiovascular disease.
CARDIOVASCULAR EXAMINATION
• Ideally the patient should be positioned lying supine with upper body resting at 45 degrees. Establish patient’s clinical stability by checking the pulse, blood pressure and pattern of breathing.
• Observe the patient’s general appearance and establish the overall level of physical comfort (dyspnoea, malaise, diaphoresis etc.), body habitus (obesity, cachexia etc.) and mental state/alertness. If obese, note where the most adiposity is distributed. Central and abdominal obesity (the so-called ‘apple’ pattern) is far more strongly associated with cardiovascular risk than obesity in the hips and periphery (the so-called ‘pear’ pattern).
• Define the rhythm, rate and character of pulse. Exclude a radial–radial or a radial–femoral delay, which can indicate the presence of a coarctation of the aorta or dissection of the aorta.
• Check the upper extremities for any peripheral stigmata of infective endocarditis (not common in contemporary practice) such as clubbing, and splinter haemorrhages. Look for palmar crease pallor indicating anaemia, and capillary return indicating sluggish circulation. Note the shape of the hand and fingers, and do not miss Marfan’s syndrome (spindle-shaped, long fingers) and acromegaly (spade-shaped, beefy hands). Exclude finger clubbing, which can be associated with subacute bacterial endocarditis or congenital cyanotic heart disease. Look for tar-stained nails, suggestive of chronic cigarette smoking.
• Assess the jugular venous pressure (JVP), its pulse morphology and check the hepatojugular reflex.
• Observe the face for any characteristic facies such as the Marfan’s face (scaphocephaly, malar hypoplasia, enophthalmos, retrognathies, down-slanting palpebral fissures), acromegalic face (protruding jaw etc.), mitral facies (pink malar discolouration of severe mitral stenosis) and Down syndrome face.
• With regard to the eyes, check for conjunctival pallor and look in the fundus for hypertensive retinal changes, diabetic retinal changes or Roth spots seen in bacterial endocarditis.
• Check the level of dental hygiene and look for the presence of gingivitis, which is associated with a higher risk of cardiovascular disease. Also exclude the presence of a high-arched palate seen in Marfan’s syndrome, and macroglossia seen in acromegaly.
• Expose the upper thorax and survey the precordium, looking for obvious apex beat, pectus excavatum or pectus carinatum, sternotomy scar (testimony to previous open heart surgery), thoracotomy scars and implanted devices such as permanent pacemakers and implanted cardiac defibrillators. Feel and locate the apex beat, and feel also for thrills and heaves. Auscultate the precordium to appreciate the heart sounds and murmurs and the radiation of the murmurs. Grade the murmur according to the loudness. Listen under the left clavicle for the machinery murmur of patent ductus arteriosus (PDA). Exclude a pericardial friction rub in the patient presenting with pleuritic precordial pain.
• Seat the patient upright and listen to the back of the thorax, looking for any evidence of pulmonary congestion in the way of mid-course crepitations. If present, define the distribution of the crepitations.
• While examining the chest, also look for pitting sacral oedema, which will be a more reliable indicator of fluid retention or cardiac failure than ankle oedema in a patient who has been supine for some time.
• Lie the patient supine and feel the abdomen in the right upper quadrant for the liver edge. Exclude painful hepatomegaly of right heart failure associated hepatic congestion and pulsatile liver of severe tricuspid regurgitation. Exclude shifting dullness of the abdomen in the patient with signs of heart failure.
CLINICAL ASSESSMENT OF THE CARDIOVASCULAR SYSTEM IN PATIENTS PRESENTING WITH POTENTIAL CARDIAC EVENTS
• Check the patient’s vital signs:
• blood pressure—look for hypertension (> 140/90 mmHg), hypotension (< 100/50 mmHg), pulsus paradoxus (weakening of pulse volume and drop in systolic blood pressure of > 10 mmHg with inspiration) or postural drop (any drop in blood pressure with standing up)
• If possible, an urgent electrocardiogram (ECG) should be performed to ensure that the patient is not having a myocardial infarction or an unstable and abnormal cardiac rhythm. If the patient presents with chest pain and the ECG shows ST segment elevation in at least two contiguous leads or a new left bundle branch block, it should be considered an acute transmural myocardial infarction and as such look at organising urgent reperfusion therapy (discussed later in this chapter). Unstable cardiac rhythms include severe bradycardia, supraventricular tachycardia (SVT), ventricular tachycardia (VT) and ventricular fibrillation.
• If there is any element of clinical instability, such as severe bradycardia (heart rate < 40 beats per minute), severe tachycardia (heart rate > 100 beats per minute) or cardiogenic shock, urgent remedial measures should be put in place and if necessary basic or advanced life support should be initiated immediately, and urgent retrieval to a hospital emergency room should be organised.
Urgent steps to be taken in this setting include the following:
Once the patient’s clinical stability is established, a more thorough assessment can be started.
CARDIOVASCULAR INVESTIGATIONS
Following is a list of common cardiac investigations with indications:
• ECG—for patients presenting with syncope, presyncope, palpitations, chest pain, hypertension, high cardiovascular risk (multiple coronary risk factors) or dyspnoea.
• Exercise stress test / myocardial perfusion scan / exercise stress echocardiogram—for patients presenting with chest pain on exertion, and those with coronary risk factors commencing on a physical activity program.
• Transthoracic echocardiogram (TTE)—for patients with cardiac murmurs, dyspnoea, chronic hypertension, syncope (to exclude severe left ventricular failure, which can lead to malignant ventricular tachyarrhythmias, or critical aortic stenosis, which can cause syncope). Also useful in those with unexplained fevers (to exclude bacterial endocarditis), hypotension with evidence of cardiac tamponade (Kussmaul’s sign—rising of JVP with inspiration, pulsus paradoxus), and after a myocardial infarction to define any regional wall motion abnormalities of the ventricles.
• Transoesophageal echocardiogram (TOE)—to exclude a patent foramen ovale (PFO) in patients presenting with a cryptogenic stroke, suspected bacterial endocarditis (small vegetations may not be detected in TTE), or to exclude thrombus in the left atrial appendage in patients who have atrial fibrillation (with stroke or prior to direct current cardioversion).
• Coronary angiography—for patients presenting with acute myocardial infarction, those with post-infarction angina, those with stable angina and a positive exercise stress test or perfusion scan, those presenting with evidence of heart failure possibly due to coronary ischaemia, and those patients who are due to undergo open heart surgery for valvular disorders.
RISK FACTORS FOR CARDIOVASCULAR DISEASE
Modifiable coronary risk factors include:
Psychological factors such as chronic stress and depression can contribute significantly to the aetiology and progression of cardiovascular disease, largely due to their association with sympathetic nervous system over-activation and high allostatic load. These effects are summarised in Figure 25.2.
PRIMARY PREVENTION
Primary prevention of acute myocardial infarction requires first and foremost the clear identification of the patient’s global risk factor profile. Once this is accomplished, the patient’s risk level can be quantified using a coronary risk calculator. The New Zealand risk score and the Framingham risk score are two such practical tools widely used in the primary care setting (Figs 25.3 and 25.4).
DIABETES MELLITUS
• Diabetes increases the cardiovascular risk two- to three-fold. Strict control of blood sugar levels, however, has not shown to be beneficial in the prevention of cardiac events and, in fact, too tight control is associated with a slightly increased risk of mortality.
• However, good blood sugar control helps in the prevention of microvascular complications such as diabetic nephropathy, neuropathy and retinopathy. It is important to aggressively control other cardiovascular risk factors in the diabetic patient.
HYPERCHOLESTEROLAEMIA
• A high total cholesterol (TC) level, high LDL cholesterol level, low HDL cholesterol level and high TG level are associated with increased coronary risk.
• In the management of high cholesterol levels, lifestyle measures such as dietary discretion, increased physical activity and weight loss should be given first priority. Those who fail lifestyle modification or those at high overall cardiovascular risk can be commenced on lipid-lowering therapy. Although they do not reduce lipid levels as significantly as some pharmaceuticals, omega-3 fatty acids are most effective in reducing cardiac and all-cause mortality. For LDL lowering, statins remain the most potent class of drugs, but they have significant side effects, such as muscle pain and weakness, and reduced cognitive ability. Many patients resist prescription of statins because of concern about side effects. It is important that the patient is offered an alternative plan in addition to lifestyle measures, including:
• niacin and fibrates—useful for raising HDL, although these have less impact on reducing overall mortality; for lowering triglycerides, strict glycaemic control, fish oil supplements and fenofibrate therapy are useful
• dietary fibre—several studies have shown that soluble fibre (found in beans, oats, barley, apples, Psyllium7 and flaxseed) lowers LDL cholesterol and triglycerides
• dietary soy—20 to 50 g/day of dietary soy (tofu, miso, tempeh) can lower total cholesterol, LDL and triglycerides
• red yeast rice—(Monascus purpureus, 1200 mg b.i.d.); several studies indicate that a proprietary form of red yeast can lower cholesterol levels
• coenzyme Q10—may be depleted in patients who take statins; may help reduce the adverse effects of statins
• It is important to note that approximately 40% of patients who are eligible for lipid-lowering therapy do not get treated in the primary care setting and, of those who are treated, approximately 50% fail to reach target levels.8
• Current consensus on target lipid levels is as follows:9
| total cholesterol level | < 4 mmol/L |
| LDL cholesterol level | < 2.5 mmol/L |
| HDL cholesterol level | > 1 mmol/L |
| TG level | < 1.5 mmol/L |
HYPERTENSION
• The World Health Organization has defined systolic blood pressure > 140 mmHg and diastolic blood pressure > 90 mmHg as hypertension. In diabetic patients and those who have had a previous myocardial infarction, this cut-off is brought down to 130/85 mmHg.
• Studies of older patients indicate that blood pressure goals that are appropriate for younger patients do not provide added benefits. Treatment regimens to attain such strict blood pressure control can be associated with significant side effects, including drug interactions, postural hypotension and falls. Older patients therefore often do better with more liberal blood pressure targets.
• Over 90% of adult patients with hypertension do not have an underlying cause and therefore have essential hypertension. Although it is said that there is no ‘underlying cause’, a number of factors contribute to the development of essential hypertension, including overweight and obesity, alcohol abuse, excess dietary salt, physical inactivity and psychological factors such as emotional stress, depression and chronic anger. The remainder have secondary hypertension due to multiple possible causes such as obstructive sleep apnoea, obesity, alcohol, renal disease, renal artery stenosis, Cushing’s syndrome, Conn’s syndrome, phaeochromocytoma or acromegaly. A number of medications are also associated with causing or exacerbating hypertension, such as steroids, non-steroidal anti-inflammatories, cocaine, nicotine and licorice (Glycyrrhiza glabra).
Left untreated, hypertension can lead to disorders of various organ systems (target organ damage).
• Heart—chronic hypertension can cause left ventricular hypertrophy, diastolic heart failure, systolic heart failure, coronary artery disease and myocardial infarction.
• Eyes—hypertension can lead to retinal changes and bleeding into the retina, eventually leading to papilloedema in its most severe form.
• Arterial system—hypertension can lead to arteriosclerosis and aneurysm formation, leading to their rupture.
Investigations
• For the definitive diagnosis of hypertension, high blood pressure reading should be recorded on three occasions separated in time.
• 24-hour ambulatory blood pressure monitoring has become popular and has proved to be a more accurate and comprehensive way of diagnosing hypertension. Usually the systemic pressure should drop by about 5–10 mmHg in the early hours of the night. Absence of this nocturnal dip is associated with increased cardiovascular risk.
Management
A medication review for pro-hypertensive agents (see Boxes 25.1 and 25.2) needs to be performed.
First-line
• Diet—ensure adequate fruit and vegetables, nuts and fish (e.g. oily fish such as tuna, salmon and mackerel) at least twice a week and adequate intake of calcium.
• Fish oil—reduces all-cause cardiovascular mortality; also reduces incidence of postoperative fibrillation when used prior to cardiac surgery.
• Coenzyme Q10—CoQ10 supplements can result in a mean decrease in systolic (16 mmHg) and diastolic (10 mmHg) blood pressure.11
Dose: 100–150 mg daily; well tolerated and no known cardiac interactions.
• Hawthorn—has a positive inotropic action, increases coronary blood flow, reduces myocardial oxygen demand and has hypotensive, lipid-lowering and anti-arrhythmic effects; has a low incidence of side effects and is well tolerated. It may potentiate the effect of antihypertensive drugs, so monitor drug dose and modify accordingly.
• Garlic—a meta-analysis of clinical trials concluded that garlic is superior to placebo in the treatment of hypercholesterolaemia, but clinical significance is limited by the size of the effect.12 The small effect on cholesterol is also reflected in the 2007 review by Pittler.13 Subsequent to Pittler’s ambivalence regarding the effect of garlic on blood pressure, two other meta-analyses published in 2008 reported strong evidence for reduction of SBP and DBP in hypertensive patients.14,15 Lower levels of evidence such as traditional usage, in vitro and animal studies have alluded to other effects, such as antioxidant, anti-atherosclerosis, antiplatelet, antibacterial, antifungal, antiviral, anti-parasitic, anti-neoplastic, fibrinolytic and immunostimulant, but robust clinical trials to study the mentioned effects are still lacking.
• Green tea—green tea extract has been shown to prevent hypertension and target organ damage induced by a high angotensin II dose, likely by prevention or scavenging of superoxide anion generation.16 One prospective cohort study reported decreased relative risk of death from CVS disease in participants who consumed more than 10 cups of tea compared with those who consumed fewer than three cups.17
Dose: 3–10 cups green tea per day
• Magnesium citrate—360–600 mg daily; magnesium supplementation produces a modest, dose-dependent antihypertensive effect, according to a meta-analysis.18
Pharmaceutical
Common pharmaceutical agents used in the treatment of hypertension:
• Thiazide diuretics—a cheaper agent with moderate potency in lowering blood pressure. Caution should be exercised in diabetic patients, whose blood sugar control may be disrupted. A suitable first-line agent for the elderly patient.
• Calcium channel blockers (CCBs)—non-dihydropyridine CCBs are effective antihypertensive agents but can cause bradycardia and worsen heart failure. Dihydropyridine CCBs are useful antihypertensive agents with antianginal properties and do not cause bradycardia. These agents, however, can cause ankle oedema.
• Angiotensin-converting enzyme (ACE) inhibitors—very effective and potent antihypertensive agents with beneficial effects in ischaemic heart disease, heart failure and diabetes mellitus. Side effects include dry cough, angio-oedema, hyperkalaemia and postural hypotension.
• Angiotensin II receptor blockers (ARBs)—effective antihypertensive agents with protective effects in heart failure and diabetes.
• Combinations of ACE inhibitors or ARBs with a CCB or a thiazide diuretic in one pill can be used when a single agent fails to control blood pressure effectively. Some evidence suggests superior clinical benefits of the former combination.
• Aldosterone antagonist spironolactone is also used as an antihypertensive agent; however, worsening of renal function and hyperkalaemia should be watched for.
• According to the National Heart Foundation Guidelines of 2008, ACEs, ARBs and thiazide diuretics are to be considered first-line pharmaceutical agents.19 In cases of resistant hypertension, further investigations should be carried out to exclude a secondary cause such as renal artery stenosis or hyperaldosteronism.
POOR MENTAL HEALTH
Psychological strategies that are effective in improving mental health have also been shown to be associated with a reduced incidence of recurrence and cardiac mortality. Including psychological and social support in the management of heart disease produces major reductions in disease progression and the number of deaths.20 A review of the evidence by Linden and colleagues found that, compared to those who were given psychosocial support, those with no such support were 70% more likely to die from their heart disease and 84% more likely to have a recurrence.20 Managing depression with antidepressants has not been shown to produce a significant reduction in cardiac risk and, in fact, many of the earlier classes of drugs increased cardiac risk.
CARDIOVASCULAR DISEASES
ISCHAEMIC CHEST PAIN
Chronic stable angina
History
• Define the patient’s angina distance and ask whether this has shortened and, if so, over what time frame.
Investigations
Perform a standard cardiovascular examination.
• Exercise stress test—has good sensitivity and specificity in the high-risk population. It is not a useful test if the patient’s pre-test probability of coronary artery disease is low. Exercise echocardiogram is preferable in women as stress ECG has a higher rate of false positives in women than in men.
• Exercise or dobutamine stress echocardiogram—has a higher sensitivity and specificity than the stress test in identifying reversible coronary ischaemia.
• Myocardial perfusion scan (radionucleoid scan)—has higher sensitivity and specificity than exercise stress testing in identifying reversible coronary ischaemia. Fixed perfusion defects indicate non-viable myocardium.
Management
• Lifestyle change—patients should be encouraged to make sustained lifestyle changes such as smoking cessation, diet, physical exercise as tolerated within the levels of comfort, and stress management.
• Other aspects of a person’s life might need to be looked at, such as mental health, employment, social activities and relationships.
• Initially the patient could be managed with antianginal therapy: topical or oral nitrates, beta-blockers, calcium channel blockers or ACE inhibitors.
• If the non-invasive test is positive for reversible coronary ischaemia, the patient should be referred for coronary angiography.
• If suitable, the patient should be treated with coronary revascularisation via balloon angioplasty and stent placement, or by referral for coronary artery bypass surgery.
• Patients with left main coronary artery disease or three vessel (left anterior descending, left circumflex and the right coronary) coronary disease benefit from bypass surgery.
• Patients who are not amenable to mechanical coronary revascularisation need optimal medical therapy.
• Recalcitrant angina can be treated with second-line antiangina agents such as nicorandil, perhexiline and ivabradine.
• L-carnitine (2 g daily)—controlled studies have indicated that L-carnitine supplements increase exercise tolerance and reduce frequency of angina attacks, enabling some patients to reduce reliance on nitrates.21
Acute coronary syndrome: unstable angina and myocardial infarction
History
• Take a rapid focused history, first asking about the onset of symptoms and associated symptoms such as diaphoresis and nausea/vomiting. Check the triggers of the pain. Check the details of the pain: severity, location, radiation and relieving factors. Classic angina is retrosternal in location with radiation along the arms unilaterally or bilaterally. It may also radiate up the neck. It is described as a dull ache akin to ‘heaviness’ or a crushing sensation with no respiratory variation of its severity. Patients may experience diaphoresis and/or nausea. These features should alert to the very high likelihood of a myocardial infarction.
• Ask about coronary risk factors. Enquire about the patient’s past history, especially cardiovascular history.
Examination
• First check the vital signs and establish haemodynamic stability. Hypotension, bradycardia, tachyarrhythmia and hypoxia are warning signs of concern. If these signs are present, upon establishing vascular access, antiplatelet therapy and fluid resuscitation (for hypotension) and diuretic therapy (frusemide 40–80 mg IV) (for hypoxia related to pulmonary congestion) should be given. Oxygen (100%) should be made available via (Hudson) mask. Aspirin 150 mg should be given orally, and organise urgent reperfusion therapy if ST segment elevation is observed in the ECG.
Investigations
• Perform a 12-lead ECG as soon as possible to confirm the diagnosis and also to define the type of infarction—ST segment elevation myocardial infarction (STEMI) or non-ST segment elevation myocardial infarction (NSTEMI), because the management of the two types is different. In NSTEMI and unstable angina, the ECG shows ST segment depression or T wave inversion
• Perform a standard battery of investigations that include the full blood count, electrolyte profile, renal function indices and cardiac biomarkers such as troponin and CK-MB (creatine kinase-MB) levels.
Management of acute myocardial infarction
• Refer the patient to the nearest hospital for urgent reperfusion therapy: thrombolysis or, if a catheterisation service is available, urgent primary angioplasty.
• If the ECG shows an NSTEMI, the patient should be anticoagulated with fractionated or unfractionated heparin to stabilise the ruptured coronary plaque.
• The patient may benefit from symptomatic therapy with morphine or glyceryl trinitrate (GTN) in tablet or topical form. Ensure that the patient is not significantly hypotensive.
• Patients also benefit from a beta-blocker agent (ensure that the patient does not have bradycardia).
• If the patient has pulmonary crepitation and is not hypotensive, give a low-dose ACE inhibitor.
• The patient will benefit from HMG-CoA reductase inhibitor (statin) therapy such as simvastatin, atorvastatin or rosuvastatin.
• Significant lifestyle changes should be advocated, with cessation of smoking, dietary modification and resumption of regular recreational physical activity—at least half an hour a day of brisk walking. Patients will find it far easier to act on lifestyle advice if attention is given to enabling factors such as stress management, behaviour change skills and goal setting.
• The patient should be referred to a cardiac rehabilitation program and should be encouraged to attend the same—without doctor’s advice the compliance rate with cardiac rehabilitation is dismal (30% or less).
• Perform an echocardiogram to assess the damage sustained and the residual ejection fraction—if there is impaired systolic function of the left ventricle, the patient may benefit from eprenolone, the new-generation aldosterone antagonist, and third-generation beta-blocker therapy.
• Ongoing angina post AMI is an indication for exercise stress testing and, if positive, for coronary angiography.
• Many patients suffer significant psychological stress with AMI and some develop ongoing subclinical depression. This is associated with a poor prognosis, and therefore it is important to identify and treat the same. Good mental health is also enormously important in helping a person to make and maintain other healthy lifestyle changes.
Preparation for coronary artery bypass surgery
In recent years the increasing incidence of high-risk and elderly patients presenting for major surgery has presented a challenge for surgeons, due to the associated increased mortality and complication rate and costs. Novel ways need to be found to improve the results of surgery in these patients. Over the past 10 years at the Alfred Hospital and the Baker Heart Research Institute in Melbourne, Australia, researchers led by Professor Franklin Rosenfeldt have developed regimens of metabolic therapy with the pyrimidine precursor, orotic acid, and the antioxidant and mitochondrial respiratory chain component, coenzyme Q10.24 Using test tube studies, animal models and human studies, they have shown that these regimens improve the response of the ageing and failing heart to hypoxia, ischaemia/reperfusion injury and aerobic stress such as occur during cardiac surgery.24–29 To these original regimens, omega-3 fatty acids (fish oil supplements) and the antioxidant alpha-lipoic acid were added in an attempt to provide better clinical outcomes. The use of coenzyme Q10 supplementation as standalone treatment was validated in a clinical trial, and the entire combination of therapeutic strategies in a 1-year pilot study.25,26,30 Compared with placebo, treated patients demonstrated improved energy production in the heart muscle, increased resistance to hypoxic stress, one-day shortened hospital stay and improved postoperative quality of life.
It is on this basis that Dr Lesley Braun and Professor Franklin Rosenfeldt developed the Integrative Cardiac Surgery Wellness Program at the Alfred Hospital, which builds research conducted on site and published studies and meta-analyses demonstrating the benefits of such programs.31–34 It also incorporates research produced by hospital-based integrative cardiology and health promotion units already established in the United States (such as the Mayo Clinic and the Cleveland Clinic).
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