Recent eLetters

When the stomach compresses the left atrium this can cause paroxysmal atrial fibrillation(1), and it can also cause syncope, the latter associated with deep S waves in Lead I, deep Q waves in lead III, and ST segement depression in leads V2 to V6(2). In the reported patient with syncope attributable to left atrial compression(the latter diagnosed by computed tomography) symptoms were associated with a fall in blood pressure to 90/60 mm Hg and tachycardia of 130 beats/min. The competing diagnoses of pulmonary embolism and relevant obstructive coronary heart disease were ruled out by computed tomography. The episode of syncope was releived by a short course of cardiac massage, and the "upside down stomach" which had caused the symptoms was respositioned by hiatoplasty and fundopexy(2) References (1) Temple IP., Schmitt M., Fox DJ Feeling the squeeze: an unusual cause of atrial fibrillation Heart 2013;99:752 (2)Zwermann L., Ritter P., Spelberg F et al Syncope due to a massive upside-down stomach J Amer Coll Cardiol 2013 doi 10.1016/j.jacc.2012.09.077

Conflict of Interest:

None declared

Dear Editor

Dr. Anderson's letter in response to this editorial seems to have over interpreted the phrase 'naked eye'. I used the phrase, in what I had hitherto thought was its typical application, as a figure of speech for visual perception without the aid of a means of a magnification device. I apologize that I was not aware of the apparently common ironic use of the phrase in developmental cardiac anatomy.

Dr. Anderson is correct that without specific stains there are no reliable physical landmarks to identify the majority of the conduction system. However, with the requisite vital dyes or or post-vital stains most of the elements of the conventional conduction system in humans can be observed without magnification aids (eg in the operating room or in the autopsy suite). Indeed, much of this work is based directly on Anderson's seminal contributions.

Finally, my description of these structures was intended solely to indicate that our current conception of the cardiac conduction system, and of cardiac connectivity in general, is constrained by macroscopic and microscopic morphology (onto which the surface ECG has been retrofitted) and would benefit from additional functional annotation. This synergy between structure and function has not been lost on investigators working on the 'connectome' in the central nervous system where traditional neuroanatomy has begun to be revolutionized by cellular resolution anatomic and physiologic studies. I think a similar effort in cardiology would be powerful.

Yours sincerely

Calum MacRae

Conflict of Interest:

I am the author of the original article

The corollary to the association of incident heart failure and an increase in serum gamma glutamyl transferase(GGT)(1) is that fluctuations in the severity of heart failure might, also, have the potential to trigger fluctuations in blood levels of this parameter. Fluctuations in serum GGT levels(including restoration to the normal range) also occur during the course of the natural history of choledocholithiasis(CDL), even when calculi are still retained within the common bile duct(CBD)(2). The latter phenomenon is a confounding factor for identification of CDL when the latter co-exists with congestive heart failure(CHF), as might well be the case in patients of mean age 56.5 years(3).In the latter study 6.8% of 73,064 patients with a discharge diagnosis of uncomplicated CDL were also documented as having coexisting CHF(3). In the same study there were 15, 121 patients in whom CDL had been complicated by the development of cholangitis. Coexisting CHF was documented in 12.5% of those 15,121 patients with complicated CDL(cCDL). Acute pancreatitis was documented in the other 38,953 patients with cCDL. Congestive heart failure coexisted with cCDL in 6.8% of patients in the latter subgroup. The transition from uncomplicated CDL to cCDL is one which ocurs at the rate of 0.8% per year(3), clearly signifying that CDL is a "ticking time bomb" which, in CHF patients, mandates a heightened index of suspicion, not only for coexisting CDL,but also for cCDL. Given the fact that coexisting CHF was more prevalent in choangitis patients than in patients with acute pancreatitis(12.5% vs 6.8%) it may well be that even more vigilance is required for stigmata of cholangitis, such as increased levels of inflammatory markers, and unexplained pyrexia, in CHF patients with raised serum GGT than in counterparts with normal GGT. What also needs to be recognised is that, even when GGT has reverted to the normal range, the occasional patient with cholangitis may still have retained CBD calculi(2). References (1)Wang Y., Tuomilehto J., Jousilahti P et al Serum gamma-glutamyl transferase and the risk of heart failure in men and women in Finland Heart 2013;99:163-167 (2)Jolobe OMP Limitations of gammaglutamyl transaminase as an indicator of biliary obstruction(letter) European Journal of Internal Medicine 2012;23:e75 (3) Kummerow KL., Shelton J., Phillips S et al Predicting complicated choledocholithiasis Journal of Surgical research 2012;177:70-74

Conflict of Interest:

None declared

I read with interest the recent papers and editorial concerning elevated levels of troponin in chronic obstructive pulmonary disease (COPD) (references - 1: S?yseth V et al, Acute exacerbation of COPD is associated with fourfold elevation of cardiac troponin T, Heart 2013;99:2 122-126; 2: Stone IS et al, Raised troponin in COPD: clinical implications and possible mechanisms, Heart doi:10.1136/heartjnl-2012- 302969; and 3: Neukamm AMC et al, High-sensitivity cardiac troponin T levels are increased in stable COPD, Heart heartjnl-2012-303429Published Online First: 12 January 2013 doi:10.1136/heartjnl-2012-303429). The authors proffered a variety of possible mechanisms which could account at least in part for the troponin rises detected in instances of both acute exacerbation of COPD and stable COPD, but appear to have overlooked the possibility of right ventricular myocardial necrosis and inflammation thought secondary to increased right ventricular stretch and strain - as described by myself and co-workers in a previous article (4: Orde MM et al, Myocardial pathology in pulmonary thromboembolism, Heart 2011;97:1695- 1699). As alluded to in that paper, we are also aware of instances in which similar right ventricular myocardial necroinflammatory changes were identified in the absence of pulmonary thromboembolism (PTE), but in which there were other potential causes of increased right ventricular strain. COPD in both stable and acute guises would of course have such potential, by way of hypoxic pulmonary vasoconstriction and increased right ventricular afterload. Indeed, perhaps rather fortuitously, routine autopsy histology undertaken by myself only today - on a case with clinically significant COPD and marked pathological changes of chronic bronchitis and emphysema but only mild coronary artery disease - demonstrated quite florid changes identical with those previously described by us in instances of PTE. This proposed hypothesis explaining the elevated levels of cardiac biomarkers detected in COPD sufferers seems entirely plausible, and there is a sound evidence base to suggest that this mechanism is indeed operative in such instances.

Conflict of Interest:

None declared

We read with interest the recent multicentre UK study by Sandercock and colleagues1 quantifying prescribed exercise volume and changes in cardiorespiratory fitness (CRF) involving 950 patients across four UK outpatient cardiac rehabilitation (CR) centres routinely performing CRF testing pre- and post-CR and with clinical practice consistent with professional body guidelines. The authors characterise low volume exercise training programmes across the four rehabilitation centres - with patients receiving a modal value of 8 exercise sessions (range 6-16). This appears in stark contrast to the international studies outlined in the author's earlier systematic review and evidence-based guidelines2. Although CRF improvements varied by rehabilitation centre and testing protocol (treadmill test protocol was a significant source of the between- trial heterogeneity), the overall improvement in CRF (0.52 METS) was only one third the mean estimate reported in their earlier meta-analysis (1.55 METs)2. The authors indicated that if representative of UK services, these low training volumes and small increases in CRF may partially explain the reported inefficacy of UK CR to reduce patient mortality and morbidity, as outlined by the RAMIT group3.

We agree with the assertion that lower exercise training volumes may be partly responsible for the lower than expected CRF values reported in the UK centres evaluated. Indeed, the CRF improvements within UK centres reported by Sandercock and colleagues1 are not consistent with data observed in our community-based CR investigations (Heartwatch, Leeds Leisure Services) using submaximal (85% age-predicted maximum heart rate) exercise testing protocols to evaluate short (3 month) and longer-term (15 month) community-based exercise training in a large, representative sample of patients with cardiovascular disease. We hereby report unpublished observations of 139 patients (79% males; mean age 62 (8) years); BMI 28 (4) kg*m-2; 62% on beta-blockers) who undertook 3 months of structured exercise-based community CR (undertaking a minimum of 2 circuit training sessions per week). Pre and post-CR exercise testing at the Heartwatch Centre was conducted on a Marquette treadmill using a specifically designed 2-minute stage incremental walking protocol4. The oxygen consumption at stages 5 and 6 (10 to 12 minutes duration) of the protocol was an estimated 25 to 29 ml?kg-1?min-1. Patients were encouraged to exercise up to 85% of age-predicted maximum heart rate (220?age) or a "very hard" rating of perceived exertion (RPE 17) using the Borg scale. Following 3 months exercise training, surrogate CRF variables including exercise duration (10.1 ? 2.5 min v 11.5 ? 2.7 min; P=0.0001) significantly improved. These improvements in submaximal CRF are consistent with our earlier reported observations5 among 154 non-diabetic CVD patients (89% male; aged 60 ?9 years; body mass index [BMI], 27?4 kg?m -2) who completed a further 12 months of exercise training. Self-reported exercise training compliance rates at 15 months, reported on clinical reassessment was 2.9 ?0.9 sessions per week. Exercise test results showed that submaximal treadmill duration increased from 10.1 to 12.2 minutes. These short and longer term improvements in CRF to graded walking represented an additional 2-minute stage of the incremental walking protocol4, corresponding to a 1.0 MET improvement in CRF.

We also feel that the methods used to estimate exercise training volumes and the impact this may have on exercise prescription may also be contributory factors in many UK-based CR programmes. The prescription of an appropriate exercise dose should be predicated on a clear appreciation of patient requirements and their physical characteristics including the degree of cardiac dysfunction and level of skeletal muscle wastage. Exercise intensity thresholds should be high enough to be effective but should be titrated within appropriate safety margins. Therefore, CRF should be assessed as accurately possible in cardiac populations. In the UK, there has arguably been a historical over-reliance on exercise prescription derived from indirect, submaximal assessments of exercise capacity, such as the incremental shuttle walk test (ISWT) and/or 6-minute walk tests (6-MWT) in patients undertaking CR. This observation was clearly evident in the recent publication by Dr Sandercock and colleagues1 who reported the use of these assessment modalities in four audited centres (treadmill and cycle ergometry were also used in two centres). Many UK centres will then use performance from submaximal tests to inform exercise training prescription relying solely on using predicted heart rate training zones and/or ratings of perceived exertion. Clearly, submaximal exercise test protocols do not rigorously evaluate the integrity of the cardiorespiratory system (a primary purpose of the exercise test). Therefore, it is possible that patient effort may be more variable in submaximal, self-paced tests such as the 6-MWT. Consequently, the widespread practice of submaximal exercise testing in the UK may be one of the reasons why CR programmes appear to be less effective.

In Europe and North America there is a much greater focus on "gold standard" techniques, including maximal exercise testing with metabolic gas exchange (cardiopulmonary exercise testing) which provide the preferred method for assessing CRF and prescribing exercise training in CR. Exercise prescription may be fine-tuned on the ventilatory anaerobic threshold or respiratory compensation point. There is overwhelming evidence indicating the superior prognostic value of ventilatory markers including peak oxygen uptake, VE/VCO2 slope, and exertional oscillatory ventilation, amongst others, especially in lower functional capacity groups such as chronic heart failure6. Ventilatory markers are rarely assessed and are seldom considered during exercise prescription in the majority of CR programmes in the UK.

Under certain circumstances, there may be a requirement to assess individual responses to exercise with submaximal testing protocols. For example, if the assessment of exercise capacity is undertaken outside a hospital setting (sporting or community centre); if a medical doctor is not available to supervise the maximal test; or when a large number of patients require assessment over a short time frame. If maximal exercise testing is to become more pervasive in the UK there will be a requirement for an initial capital outlay on equipment (though existing testing systems may be under-utilised in many Trusts around the country), and there will be a need for specialist staff training and on-going consumable costs. However, we should not lose perspective over the major objectives of CR, the Cinderella of cardiology services, and bear in mind the apparent under-prescription of exercise that seems to be common practice in UK centres. UK-based CR should not be run on a shoe-string budget. It has been long-established that increasing CRF reduces mortality and morbidity in secondary prevention settings7. There is a pressing need to adopt a more evidence-based approach to exercise prescription in patients undertaking CR in the UK.

Dr Lee Ingle & Professor Sean Carroll Department of Sport, Health & Exercise Science University of Hull Kingston-upon-Hull HU6 7RX United Kingdom

References:

1. Sandercock GR, Cardoso F, Almodhy M, Pepera G. Cardiorespiratory fitness changes in patients receiving comprehensive outpatient cardiac rehabilitation in the UK: a multicentre study. Heart. 2012 Nov 24. [Epub ahead of print].

2. Sandercock G, Hurtado V, Cardoso F. Changes in cardiorespiratory fitness in cardiac rehabilitation patients: A meta-analysis. Int J Cardiol. 2011; [Epub ahead of print].

3. West RR, Jones DA, Henderson AH. Rehabilitation after myocardial infarction trial (RAMIT): multi-centre randomised controlled trial of comprehensive cardiac rehabilitation in patients following acute myocardial infarction. Heart 2012; 98(8):637-44.

4. Lehmann G, Schmid S, Ammer R, Sch?mig A, Alt E. Evaluation of a new treadmill exercise protocol. Chest1997;112(1):98-106.

5. Carroll S, Tsakirides C, Hobkirk J, Moxon JW, Moxon JW, Dudfield M, Ingle L. Differential improvements in lipid profiles and Framingham recurrent risk score in patients with and without diabetes mellitus undergoing long-term cardiac rehabilitation. Arch Phys Med Rehabil 2011;92(9):1382-7.

6. Arena R, Myers J, Williams MA, et al. Assessment of functional capacity in clinical and research settings: A scientific statement from the American Heart Association Committee on Exercise, Rehabilitation, and Prevention of the Council on Clinical Cardiology and the Council on Cardiovascular Nursing Circulation. 2007;116: 329-343.

7. Vanhees L, Fagard R, Thijs L, Amery A. Prognostic value of training-induced change in peak exercise capacity in patients with myocardial infarcts and patients with coronary bypass surgery. Am J Cardiol 1995; 15; 76(14):1014-9.

Conflict of Interest:

None declared