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Recommendations for combined valve surgery and coronary artery bypass grafting

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Recommendations for combined valve surgery and coronary artery bypass grafting

Overall the prevalence of valvular heart disease is rising as the general population ages. Accordingly, the risk profile of patients undergoing surgery is increasing. The consequence of this change is that some patients requiring valve replacement and CABG may represent too high a risk for a single combined operation. Alternative treatments include using ‘hybrid’ procedures, which involve a combination of both scheduled surgery for valve replacement and planned PCI for myocardial revascularization. At present, however, the data on hybrid valve/PCI procedures are very limited, being confined to case reports and small case series [ 143 ]. Another option that may be considered in these high-risk surgical patients is transcatheter aortic valve implantation [ 144 ].

The incidence of significant carotid artery disease in patients scheduled for CABG depends on age, cardiovascular risk factors, and screening method. The aetiology of post-CABG stroke is multifactorial and the main causes are atherosclerosis of the ascending aorta, cerebrovascular disease, and macroembolism of cardiac origin. Carotid bifurcation stenosis is a marker of global atherosclerotic burden that, together with age, cardiovascular risk factors, previous stroke or transient ischaemic attack (TIA), rhythm and coagulation disturbances, increases the risk of neurological complications during CABG. Conversely, up to 40% of patients undergoing carotid endarterectomy (CEA) have significant CAD and may benefit from pre-operative cardiac risk assessment [ 123 ].

The incidence of perioperative stroke after on-pump CABG varies from 1.5% to 5.2% in prospective studies and from 0.8% to 3.2% in retrospective studies. The most common single cause of post-CABG stroke is embolization of atherothrombotic debris from the aortic arch, and patients with carotid stenosis also have a higher prevalence of aortic arch atherosclerosis. Although symptomatic carotid artery stenosis is associated with an increased stroke risk, 50% of strokes after CABG do not have significant carotid artery disease and 60% of territorial infarctions on computed tomography (CT) scan/autopsy cannot be attributed to carotid disease alone. Furthermore, only 45% of strokes after CABG are identified within the first day after surgery while 55% of strokes occur after uneventful recovery from anaesthesia and are attributed to AF, low cardiac output, or hypercoagulopathy resulting from tissue injury. Intraoperative risk factors for stroke are duration of cardiopulmonary bypass (CPB), manipulation of the ascending aorta, and arrhythmias. Off-pump CABG has been shown to decrease the risk of stroke, especially when the ascending aorta is diseased, and particularly if a no-touch aorta technique is used.

In this regard, we have previously suggested that uric acid may have had a significant role in mediating the marked rise in hypertension prevalence that has occurred worldwide [ 42 ]. Over the last century, there has been a dramatic increase in the ingestion of added sugars which contain fructose, and the increased consumption of added sugars correlates both with higher serum uric acid levels and with elevated blood pressure [ 43,44 ]. Administering high doses of fructose to humans raises uric acid levels and blood pressure, and preventing the rise in uric acid with allopurinol prevents the increase in blood pressure [ 45 ]. Diets restricting fructose also lower uric acid levels and blood pressure (M. Madero, submitted). Mean serum uric acid levels are also increasing in our population in association with the rise in fructose ingestion and increasing prevalence of hypertension, and numerous studies have found that elevated uric acid could predict the development of hypertension [ 46,47 ]. Additionally, several small clinical trials have reported that lowering uric acid could reduce blood pressure in humans, including a recent prospective double-blind trial in obese adolescents [ 48–50 ]. Clearly, additional studies are required to confirm these findings.

As mentioned, a number of epidemiologic and experimental studies have shown that increased dietary fructose intake, particularly in the form of high-fructose corn syrup, (HFCS) is associated with development of hyperuricaemia. The precise mechanism by which fructose causes an increase in uric acid relates to its unique metabolism. The initial phosphorylation of fructose to fructose-1-phosphate by fructokinase results in adenosine triphosphate (ATP) consumption. Unlike glucokinase, which has a negative feedback to prevent excessive phosphorylation and ATP depletion, the phosphorylation of fructose will proceed until all fructose is phosphorylated. During this process, intracellular phosphate falls, and adenosine monophosphate (AMP) deaminase is stimulated, which results in the production of inosine monophosphate (IMP) and eventually uric acid. Intracellular uric acid rises followed by a rise in serum uric acid that peaks at ~ 30min [ 51,52 ]. With high levels of fructose ingestion, even fasting levels of uric acid will rise, consistent with epidemiological studies linking fructose intake with hyperuricaemia [ 53 ].

The arterioles have a major role in protecting distal organs from the elevated pressure present in the central circulation. In the kidney, this autoregulatory vasoconstrictive response is critical in preventing transmission of pressure to the glomeruli and peritubular capillary bed. Bidani and Griffin have provided convincing evidence that an altered renal autoregulatory response is commonly present in chronic kidney disease, and that this leads to increased transmission of systemic pressure to the glomeruli [ 54 ]. An insight into the mechanism was provided by the laboratory of the late Jaime Herrera-Acosta, who showed that the development of afferent arteriolar disease resulted in impaired autoregulation and glomerular hypertension [ 14 ]. Importantly, this group showed that if the arteriolosclerosis could be prevented and renal autoregulation remained intact, the progression of renal disease could be halted [ 14 ]. The mechanism is relatively logical, for the diseased arterioles have been shown to have an increase in collagen content [ 10 ] and hence are not expected to vasoconstrict or vasodilate as quickly or as efficiently as normal arterioles. We have suggested that the consequences of altering the autoregulatory mechanisms of the arteriocapillary bed may be critical as a risk factor for end-organ damage, particularly by increasing the risk for progression of renal disease [ 14 ]. This concept has also been proposed for the impairment of brain function by Thompson and Hakim in a recent publication [ 55 ].

Treatment of orthostatic hypertension

BP = blood pressure; OH = orthostatic hypertension; PCM = physical counter-pressure manoeuvres.

a
b

Treatment of orthostatic hypertension

BP = blood pressure; OH = orthostatic hypertension; PCM = physical counter-pressure manoeuvres.

a
b

Current management strategies in patients with syncope due to intrinsic cardiac bradycardia are summarized in Figure 13 .

Figure 13
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Summary of indications for pacing in patients with syncope due to intrinsic cardiac bradycardia. AF = atrial fibrillation; asympt. = asymptomatic; AV = atrioventricular; BBB = bundle branch block; ECG = electrocardiogram; EPS = electrophysiological study; HR = heart rate; ILR = implantable loop recorder; SB = sinus bradycardia; SND = sinus node dysfunction; sympt. = symptomatic.

Figure 13
View large Download slide

Summary of indications for pacing in patients with syncope due to intrinsic cardiac bradycardia. AF = atrial fibrillation; asympt. = asymptomatic; AV = atrioventricular; BBB = bundle branch block; ECG = electrocardiogram; EPS = electrophysiological study; HR = heart rate; ILR = implantable loop recorder; SB = sinus bradycardia; SND = sinus node dysfunction; sympt. = symptomatic.

In general, cardiac pacemaker therapy is indicated and has proved effective in intrinsic sinus node disease when intermittent sinus arrest or sinoatrial block has been demonstrated to account for syncope by means of ECG documentation during spontaneous syncope. 334–338 A frequent situation is that of patients who have prolonged sinus pause following the termination of tachycardia in bradycardia−tachycardia syndrome due to the abnormally prolonged time needed for the recovery of automaticity by a diseased sinus node. Permanent pacing does not affect survival.

When the correlation between symptoms and ECG is established, there is general consensus that cardiac pacing is effective and useful for symptom relief.

In the absence of the above situations, despite adequate pacing, syncope recurs in approximately 15–28% of patients at 5 years 339–341 (see adidas Men’s Response 3 M Running Shoes Grey Blue White Aq2498 cheap sale geniue stockist cheap sale wiki clearance finishline 2kKNKc
). This is due to the frequent association of a vasodepressor reflex mechanism with sinus node disease. In patients with sinus node disease and syncope, carotid sinus hypersensitivity and a positive response to tilt are present in ≤50% of patients. Thus, an increased susceptibility to neurally mediated bradycardia/hypotension is often the cause of syncope. 135 , 136 A reflex mechanism of syncope fits well with the unpredictable natural history of syncope recurrence. Physicians should be aware that effectiveness of therapy is not well documented in such cases. From a practical perspective, cardiac pacing may be a reasonable solution in patients affected by sinus node disease, who have had documentation of an asymptomatic ventricular pause >3 s (with exceptions for young trained persons, during sleep, and medicated patients), when a competitive diagnosis, i.e. hypotension, can be ruled out. 294 An abnormal SNRT enhances the probability of efficacy of cardiac pacing (see section 4.2.6.1). 210–212

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