Clinical Writing for Interventional Cardiologists

Clinical Writing for Interventional Cardiologists

What you will learn - hopefully! • Introduction • General principles for clinical writing • Specific techniques • Practical session: critical review of a published article • Writing the Title and the Abstract • Bibliographic search and writing the Introduction • Principles of statistics and writing the Methods • Practical session: writing the Abstract • Writing the Results • Writing the Discussion • Writing Tables and preparing Figures • Principles of peer-review • Principles of grant writing/regulatory submission • Clinical writing at a glance • Conclusions and take home messages

What you will learn • Practical session: writing the Abstract • goals of Abstract, IMRAD approach, and effective tips • hands-on session

Abstract What makes a good abstract? First you need to ask yourself what an abstract is for!

Abstract The abstract is like the whole body of a woman It may mislead, but it is decisive in making the choice for reading the full-text of the article

IMRAD algorithm Introduction (± Aim) 2-3 phrases Methods 2-3 phrases Results 3-5 phrases And Conclusions 1-3 phrases

Abstract • A good abstract should: • State the principal objectives and scope of the investigation • Describe the methods employed • Summarize the results • State the principal conclusions

Following the rules • Concise as possible, but brisk! • Body length determined • ~175-250 Words (shorter – for journals) • ~300-350 Words (longer – for congresses) • It may be difficult to comply, especially if very structured (eg JAMA, Annals of Internal Medicine)

What you will learn • Practical session: writing the Abstract • goals of Abstract, IMRAD approach, and effective tips • hands-on session

Details of hypothetical trial Design: prospective Allocation: randomized Setting: single center Time: October 2004 to July 2005 Population: Inclusion criteria were age < 75 years old with acute ST-elevation myocardial infarction (chest pain persisting ≥30 minutes was associated with ST segment elevation ≥0.1 mV in ≥2 continuous electrocardiographic leads). Clinical exclusion criteria were cardiogenic shock, thrombolytic therapy, oral anticoagulant therapy, prolonged cardiopulmonary resuscitation, previous coronary artery bypass graft (CABG), PCI or ischemic stroke within 6 months, and hemorrhagic diathesis. Angiographic exclusion criteria were previous stenting of the infarct-related artery (IRA) and a reference vessel diameter (RVD) of the culprit lesion of <2.25 mm by visual estimate. Intervention: percutaneous coronary intervention (PCI) with drug-eluting stent implantation Comparison: PCI with bare-metal stent implantation

Details of hypothetical trial Outcomes (1): The primary end-point was a percentage of the stent volume obstructed by NIH measured by IVUS at 7±1 months. Secondary end-points were 7±1 months angiographic binary restenosis rate and major adverse cardiac events (MACE), that is, any death, nonfatal myocardial infarction, and TLR at discharge, at 1 and 7±1 months of follow-up. Binary restenosiswas defined as any diameter stenosis >50% within the total analysis segment at 7±1 months of angiographic follow-up. Recurrent infarctionwas defined as the recurrence of clinical symptoms or the occurrence of electrocardiographic changes accompanied by a newelevation in the levels of creatine kinase, creatine kinase MB enzyme, or both. The level of creatine kinase required for the diagnosis of reinfarction depended on the interval from the index infarction: the creatine kinase level had to be at least 1.5 times the previous value if new symptoms appeared within 48 hours and at least three times the upper limit of normal if new symptoms appeared after 48 hours.

Details of hypothetical trial Outcomes (2): TLR was defined as any reintervention (with CABG or PCI) on the total analysis segment. Target vessel revascularization was defined as any reintervention (with PCI or CABG) on the culprit vessel. Stent thrombosis was specifically assessed and divided into acute (periprocedural), subacute (from 6 hours after procedure to 30 days), and late; acute and subacute stent thrombosis were defined by protocol as angiographic proof of vessel occlusion, any recurrent myocardial infarction in the territory of the stented vessel, or any death from cardiac causes. Late stent thrombosis was defined as any recurrent myocardial infarction with angiographic proof of occlusion in the stented vessel. The new Academic Research Consortium classification to evaluate definite, probable, and possible cases of stent thrombosis was also applied to our series in the data analysis.

Details of hypothetical trial Results (1): Patient and Procedural Characteristics: Between October 2004 and July 2005, 80 consecutive patients with STEMI were enrolled and randomized into two independent cohorts (40 in the DES and 40 in the BMS cohort). The most frequent reasons for exclusion were cardiogenic shock and previous thrombolytic therapy. The two populations were well matched for baseline and clinical characteristics. Every patient underwent successful revascularization, as shown by 100% postprocedural TIMI flow grade 3 and optimal reperfusion angiographic parameters (corrected TIMI frame count, myocardial blush grade). Significantly longer stents were deployed in the paclitaxel cohort, while lesion length at QCA was not significantly different. No episodes of acute stent thrombosis were reported in both cohorts. IVUS analysis demonstrated a very low incidence of ISA (one patient per group). Postprocedure lumen area was 8.5 mm2 in the BMS group versus 8.36 mm2 in the DES group (P=0.844).

Details of hypothetical trial Results (2): Primary End-Point: Angiographic follow-up with IVUS measurements was performed in 76 (95%) patients. Statistically significant differences favoring the DES group for the primary end-point were largely demonstrated with 4.6% NIH in the DES group versus 20% in the BMS group (P<0.001). The difference remained significant even when NIH was expressed as a difference between stent and lumen volume (9.3 vs 33.6 mm3, P<0.001). In-Hospital and Follow-Up Clinical Data: Peak CK value was comparable between the two cohorts. One in-hospital MACE was reported in each group (one subacute stent thrombosis successfully treated with PCI in the BMS cohort and one cardiac sudden death with autopsy evidence of subacute stent thrombosis in the DES cohort). Clinical follow-up at 1 month was performed in 100% of discharged patients (n=79) and no further events were adjudicated…

Details of hypothetical trial Results (3): … At 7-month follow-up, three patients had died in the BMS group (two cardiac deaths). No more episodes of reinfarction were reported, while the overall rate of TLR was 32.5% for the BMS group versus 5% for the DES group (P=0.01); among the 15 patients who underwent TLR, 6 (40%) were asymptomatic (including the two revascularizations in the DES cohort), 7 (46.7%) had a positive stress test, and 2 (13.3%) were symptomatic in presence of a positive test. The TVR rate was 42.5% in the BMS vs 17.5% in DES (P=0.05), and TLR rate 10% vs 12.5% (P=0.99), including six asymptomatic patients and three with a positive stress test. No definite or probable late stent thromboses occurred while two possible late stent thromboses were reported in the BMS cohort. Follow-Up Coronary Angiography: At online QCA performed during angiographic follow-up, instent late lumen loss was 1.01 mm vs 0.10 mm and in-segment late loss was 1.07 mm versus 0.10 mm (P=0.001); accordingly, binary restenosis occurred in 35% versus 5.1% of the patients (P=0.01)…

Details of hypothetical trial Results (4): … In-segment binary restenosis rate was 37.8% versus 5.0% (P=0.003). Restenosis patterns in the DES group were Mehran grade II (50%) and III (50%); the most frequent pattern in the BMS group was Mehran grade III (71.5%). Follow-Up Intravascular Ultrasound: IVUS analysis was performed in all patients alive at 7 months. No difference was reported in the study cohorts for vessel and stent volume, while lumen volume was greater in the DES group than in the stented segment (150.3 in BMS vs 194.2mm3 in DES, P=0.015), as was minimal lumen area (MLA) at the distal edge (6.2 in BMS vs 8.8mm2 in DES, P<0.001). A significant difference was observed in primary end-point, as well as in the MLA intrastent (4.55 vs 6.38 mm2, P=0.001). Late-acquired ISA rate was 2.7% in BMS versus 5.1% in DES (P=0.65).

Details of hypothetical trial BMS DES

Details of hypothetical trial DES BMS

Remember IMRAD Introduction (± Aim) 2-3 phrases Methods 2-3 phrases Results 3-5 phrases And Conclusions 1-3 phrases

and now let’s work!

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Clinical Writing for Interventional Cardiologists