A pilot study on the effect of advance care planning implementation on healthcare utilisation and satisfaction in patients with advanced heart failure.

BACKGROUND: Patients with advanced heart failure may benefit from palliative care, including advance care planning (ACP). ACP, which can include referral back to the general practitioner (GP), may prevent unbeneficial hospital admissions and interventional/surgical procedures that are not in accordance with the patient's personal goals of care. AIM: To implement ACP in patients with advanced heart failure and explore the effect of ACP on healthcare utilisation as well as the satisfaction of patients and cardiologists. METHODS: In this pilot study, we enrolled 30 patients with New York Heart Association class III/IV heart failure who had had at least one unplanned hospital admission in the previous year because of heart failure. A structured ACP conversation was held and documented by the treating physician. Primary outcome was the number of visits to the emergency department and/or admissions within 3 months after the ACP conversation. Secondary endpoints were the satisfaction of patients and cardiologists as established by using a five-point Likert scale. RESULTS: Median age of the patients was 81 years (range 33-94). Twenty-seven ACP documents could be analysed (90%). Twenty-one patients (78%) did not want to be readmitted to the hospital and subsequently none of them were readmitted during follow-up. Twenty-two patients (81%) discontinued all hospital care. All patients who died during follow-up (n = 12, 40%) died at home. Most patients and cardiologists indicated that they would recommend the intervention to others (80% and 92% respectively). CONCLUSION: ACP, and subsequent out-of-hospital care by the GP, was shown to be applicable in the present study of patients with advanced heart failure and evident palliative care needs. Patients and cardiologists were satisfied with this intervention.

Implications of automated creatine kinase (CK)-MM1,2,3/CK-MB1,2 isoform analysis as an early marker for the detection of myocardial tissue damage.

Measurement of creatine kinase (CK) isoforms enables the clinician to detect myocardial tissue damage at an early stage after myocardial infarction. According to the manufacturer's specifications, it should be possible to perform CK isoform analysis automatically using the new Cardio Rep analyser. In order to investigate the suitability of this new analyser we measured the CK MM1-3, and CK MB1 and 2 isoform patterns, firstly in 30 patients with acute myocardial infarction (AMI), for whom total CK and CK-MB levels were ordered, and secondly in 23 patients with chest pain suspected as having AMI (n = 11) or with unstable angina pectoris (UAP) (n = 12). The total time for analysis, including 5 min pre- and 10 min post-analyser run time, was found to be 40 min. For elevated MB2/MB1 ratios there is a discrepancy between the MB2/MB1 ratios determined from the densitometric scans concerning the surface and the peak height ratios. The MB2/MB1 ratios of the studied AMI patients exceeded the upper reference limits approximately 2 h after the onset of symptoms, whereas the CK-MB and total CK levels increased after about 6 h. The MB2/MB1 ratios from the patients with UAP were either below the detection limit or these patients could be discriminated from patients with AMI when low CK-MB and total CK levels were considered in conjunction. From our results we conclude that assessment of CK isoforms can be performed relatively simply with the new analyser within 40 min. However, for reliable calculation of the MB2/MB1 ratios, the curve monitoring of the MB2-MB1 densitometric scans should be improved. The CK isoforms are useful as an early marker for AMI as their reference interval is already exceeded approximately 2 h after an AMI. Moreover, CK isoform analysis might prove to be useful in discriminating at an early stage between AMI and other causes of chest pain. This could decrease the number of patients with a false-positive diagnosis admitted to coronary care units, resulting in a reduction of costs.

Laser thrombolysis in acute myocardial infarction: results of a clinical feasibility study.

Laser thrombolysis is a new, experimental, catheter based intervention aimed at selectively removing intracoronary thrombus. This first clinical study was performed to assess the feasibility and safety of laser thrombolysis, as well as its potential therapeutic place in acute myocardial infarction. Eighteen patients with acute myocardial infarction, who were either noncandidates for, or failures on, intravenous fibrinolytic therapy were included for treatment with laser thrombolysis followed by balloon angioplasty. As a result of catheter and technical failures, the laser was actually fired in only 12 patients. Improvement in TIMI flow from grade 0-1 to grade 2-3 was observed in 10 of these 12 patients after laser application. The overall results of 18 patients were: increase in TIMI grade flow from 0.33 +/- 0.49 after wire passage to 1.28 +/- 1.23 (P = 0.0051) after attempted laser application, and to 2.67 +/- 0.97 after PTCA (P = 0.0004). Two patients with previous infarctions died from left ventricular failure despite successful laser thrombolysis. One patient died during emergency bypass surgery after a failed recanalization attempt. Perforation or laser related dissection did not occur. The concept of selective laser thrombus ablation seems to be safe and feasible, but substantial improvements of the laser delivery catheters are needed. Laser thrombolysis is not an effective stand-alone therapy in acute myocardial infarction, but other possible applications warrant further research and development efforts for this potentially useful interventional tool.

Serial angioscopic and angiographic observations during the first hour after successful coronary angioplasty: a preamble to a multicenter trial addressing angioscopic markers for restenosis.

Percutaneous coronary angioscopy was used in 13 patients in a pilot study to assess the intracoronary changes that occur during the first hour after balloon angioplasty (PTCA). The dilated segment was studied with 4.5F angioscopes and with quantitative coronary angiography (QCA) immediately after PTCA and at 15-minute intervals for up to 1 hour after PTCA. Significant progression of intimal dissection and thrombus formation could be demonstrated with angioscopy. These dissections and thrombi remained undetected with angiography, which only showed haziness. Thus through its superior sensitivity to intimal damage and thrombus, coronary angioscopy can reveal important intravascular events that apparently occur even after successful PTCA. The relation of such angioscopic observations to restenosis will be addressed in a subsequent multicenter study.

Late onset atrioventricular nodal tachycardia.

AV nodal tachycardia may present at any age, but onset in late adulthood is considered uncommon. To evaluate whether onset of AV nodal tachycardias at older age is related to organic heart disease (possibly setting the stage for re-entry due to degenerative structural changes) 32 consecutive patients with symptomatic AV nodal tachycardia were studied. The age at onset of attacks showed a bimodal pattern, with 2 peaks: one between 15 and 35 years (22 patients) and one around 55 years (10 patients). Significantly more older patients had an underlying heart disease (60% versus 14%, P < 0.01), with coronary artery disease in 4 and hypertensive heart disease in 3. Frequent supraventricular ectopic activity was seen during baseline 24-h ambulatory monitoring in all the older patients, versus in only half of the younger patients (P = 0.005). These results indicate that late onset AV nodal tachycardia (i.e. > age 45 years) is not infrequent (33%). The frequent supraventricular arrhythmias on one hand and age-related structural AV nodal changes, potentially enhanced by underlying heart disease on the other, both may contribute to the development of late onset re-entrant AV nodal tachycardia.