When to consider an implantable cardioverter defibrillator following myocardial infarction?

After reading this article the reader should be familiar with: Current guidelines for implantable cardioverter defibrillator (ICD) use post myocardial infarction (MI) and ischaemic cardiomyopathy. Primary prevention ICD guidelines. Secondary prevention ICD guidelines. Non-sustained ventricular tachycardia in patients post MI and the use of ICDs. Programming ICDs.

Ethical and legal perspective of implantable cardioverter defibrillator deactivation or implantable cardioverter defibrillator generator replacement in the elderly.

PURPOSE OF REVIEW: Implantable cardioverter defibrillator (ICD) implantation has become a common and standard treatment for primary and secondary prevention of sudden cardiac death in patients with poor left ventricular ejection fraction across the world. Circumstances, of course, change after the initial implant as patients age. This raises legal and ethical questions about deactivating or not replacing ICD generators when the likelihood of meaningful benefit has diminished. RECENT FINDINGS: Health professionals are reluctant to discuss the end-of-life planning with patients who have ICDs. Older patients are more likely to have multiple comorbidities that worsen or accumulate further after initial implantation and attenuate the survival benefit of ICDs. Joint guidelines suggest physicians educate patients during the initial consent process about the possibility of deactivating ICDs after implantation if their individual situation changes to the point of futility. SUMMARY: ICD deactivation and nonreplacement are unavoidable issues that require clarity for meaningful and ethical implementation. This is an ongoing process.

Transseptal left ventricular lead placement using snare technique.

BACKGROUND: Coronary sinus (CS) lead placement for cardiac resynchronization therapy has a failure rate of ∼5-10%. Here we describe a way of implanting an endocardial left ventricular (LV) lead via a transseptal puncture (TSP), using a GooseNeck snare and active fixation lead. METHODS: Three male patients (67-83 years) with failed or extracted epicardial LV leads implanted via the CS had an endocardial LV lead implanted. TSP was performed via a femoral vein. The active fixation pacing lead was advanced to the right atrium from a subclavian vein. A GooseNeck snare was passed via the TSP sheath and used to grasp the tip of the pacing lead. The sheath, GooseNeck snare, and pacing lead tip were then passed to the left atrium by sliding the system up the TSP guidewire and across the interatrial septum before deflecting the lead to permit implantation in the left ventricle. RESULTS: Successful implantation was performed in all patients with an LV implant time of 25-55 minutes. CONCLUSION: The use of a GooseNeck snare via a deflectable transseptal sheath represents a reliable alternative method for endocardial LV lead placement in patients with failed CS LV lead implantation.

Development and validation of a clinical score to identify echocardiographic left ventricular hypertrophy in patients with cardiovascular disease.

BACKGROUND: Echocardiographic (echo) left ventricular hypertrophy (LVH) is an independent predictor of mortality. Despite this, screening for LVH in patients with overt cardiovascular diseases is not universally done. To help target echo screening for LVH in patient population, we developed and validated a simple clinical score to help identify those likely to have echo LVH. METHODS: We performed two studies. The development cohort consisted of 267 patients with angina. The validation cohort consisted of 227 patients with peripheral arterial disease. RESULTS: The prevalence of echo LVH in both patient cohorts was 50%. Six independent predictors of LVH were identified in the development cohort: age >65 years (1 point), body mass index >30 kg/m2 (1 point), history of hypertension (1 point), previous myocardial infarction (1 point), clinic blood pressure >130/80 mm Hg (1 point) and bundle branch block (BBB) on electrocardiogram (4 points). Our clinical score was strongly associated with the presence of LVH in the validation cohort. It also showed a significant continuous positive relationship (P trend <0.001 in males and P trend = 0.006 in females) with increasing quartiles of LV mass in both cohorts. In those without BBB, a modified clinical score performed equally well. CONCLUSION: We have developed a simple clinical score which quantifies the chance that any patient with manifest cardiovascular disease has the added risk factor of LVH. This will help target precious echo resources toward individuals who are most likely to have this condition. This could potentially lead to better risk stratification in this patient population.

Left ventricular hypertrophy is present in one-half of newly-diagnosed peripheral arterial disease patients.

OBJECTIVES: Peripheral arterial disease (PAD) patients are at high risk of cardiac death. Coincidental but silent coronary disease is obviously a major contributor but left ventricular hypertrophy (LVH) could be a second major contributor. METHODS: To investigate whether LVH could really be making a large contribution to cardiac death in PAD, we assessed the prevalence of LVH when PAD was first diagnosed. RESULTS: The prevalence of echo LVH when left ventricular mass was indexed to body surface area was 50%. Although office blood pressure and 24-h blood pressure were both significantly higher in those with LVH, in clinical practice, a contemporaneous blood pressure measurement (office or 24 h) at the time of PAD diagnosis would only partially identify those with LVH. For example, an office blood pressure cut-off of < 140/90 mmHg was found in 27% of all LVH cases and a 24-h blood pressure cut-off of < 125/80 mmHg was found in 24% of all LVH cases. CONCLUSION: In conclusion, there is already a high prevalence of LVH in patients at first diagnosis of PAD. LVH is therefore common enough in PAD patients to potentially make a major contribution to cardiac death, which means that future research should now investigate whether screening for and regressing LVH when present would actually reduce cardiac deaths over and above merely achieving target blood pressure.