Josep Guindo

Interatrial blocks. A separate entity from left atrial enlargement: a consensus report

Impaired interatrial conduction or interatrial block is well documented but is not described as an individual electrocardiographic (ECG) pattern in most of ECG books, although the term atrial abnormalities to encompass both concepts, left atrial enlargement (LAE) and interatrial block, has been coined. In fact, LAE and interatrial block are often associated, similarly to what happens with ventricular enlargement and ventricular block. The interatrial blocks, that is, the presence of delay of conduction between the right and left atria, are the most frequent atrial blocks. These may be of first degree (P-wave duration >120 milliseconds), third degree (longer P wave with biphasic [±] morphology in inferior leads), and second degree when these patterns appear transiently in the same ECG recording (atrial aberrancy). There are evidences that these electrocardiographic P-wave patterns are due to a block because they may (a) appear transiently, (b) be without associated atrial enlargement, and (c) may be reproduced experimentally. The presence of interatrial blocks may be seen in the absence of atrial enlargement but often are present in case of LAE. The most important clinical implications of interatrial block are the following: (a) the first degree interatrial blocks are very common, and their relation with atrial fibrillation and an increased risk for global and cardiovascular mortality has been demonstrated; (b) the third degree interatrial blocks are less frequent but are strong markers of LAE and paroxysmal supraventricular tachyarrhythmias. Their presence has been considered a true arrhythmological syndrome.

Recurrent pericarditis. Relief with colchicine.

Recurrence is one of the major complications of pericarditis. Treatment of recurrence is often difficult, and immunosuppressive drugs or surgery may be necessary. We conducted an open-label prospective study of nine patients (seven men and two women; age, 18-64 years; mean age, 41.7 +/- 13.7 years). Patients were treated with colchicine (1 mg/day) to prevent recurrences. All patients had suffered at least three relapses despite treatment with acetylsalicylic acid, indomethacin, prednisone, or a combination. Pericarditis was classified as idiopathic in five patients, postpericardiotomy in two, post-myocardial infarction in one, and associated with disseminated lupus erythematosus in one. For statistical analysis, we conducted a paired comparison design (Students t test). All patients treated with colchicine responded favorably to therapy. Prednisone was discontinued in all patients after 2-6 weeks (mean, 26.33 +/- 10.9 days), and colchicine alone was continued. After a mean follow-up of 24.3 months (minimum, 10 months; maximum, 54 months), no recurrences were observed in any patient; there was a significant difference between the symptom-free periods before and after treatment with colchicine (p less than 0.002). Our study suggests that colchicine may be useful in avoiding recurrence of pericarditis, although these results need to be confirmed in a larger, double-blind study.

Prevalence and Prognostic Influence of Peripheral Arterial Disease in Patients ≥40 Years Old Admitted into Hospital Following an Acute Coronary Event

OBJECTIVE A significant proportion of patients with ischemic heart disease have associated peripheral arterial disease (PAD), but many are asymptomatic and this condition remains underdiagnosed. We aimed to study the prevalence of PAD in patients with an acute coronary syndrome (ACS) and to evaluate its influence in hospital clinical outcomes. METHODS The PAMISCA register is a prospective, multicenter study involving patients >or=40 years old with ACS admitted to selected Spanish hospitals. All patients had their ankle-brachial index (ABI) measured between days 3 and 7 after the ischemic event. RESULTS 1410 ACS patients (71.4% male) were included. PAD determined by ABI was documented in 561 patients (39.8%). Factors independently related to PAD were age (OR: 1.04; 95% CI: 1.03-1.06; p<0.001), smoking (OR: 1.88; 95% CI: 1.41-2.49; p<0.0001), diabetes (OR: 1.30; 95% CI: 1.02-1.65; p<0.05), previous cardiac disease (OR: 1.54; 95% CI: 1.22-1.95; p<0.001) and previous cerebrovascular disease (OR: 1.90; 95% CI: 1.28-2.80; p<0.001). Following the ACS, an ABI<or=0.90 was associated with increased cardiovascular mortality (OR: 5.45; 95% CI: 1.16-25.59; p<0.05) and a higher risk of cardiovascular complications. CONCLUSION The prevalence of PAD in patients >or=40 years presenting with ACS is high and it is associated with increased cardiovascular risk.

Impact of Clinical and Subclinical Peripheral Arterial Disease in Mid-Term Prognosis of Patients With Acute Coronary Syndrome

Observational studies report poor prognosis of patients after acute coronary syndrome (ACS) in the presence of previous peripheral arterial disease (PAD), but data on subclinical PAD are scarce. This study was designed to assess the predictive value of clinical and subclinical PAD in the follow-up of patients after an ACS. We included 1,054 patients hospitalized for an ACS who survived the acute phase. Patients were divided into 3 groups: clinical PAD (previously diagnosed PAD or intermittent claudication), subclinical PAD (defined as ankle-brachial index <or=0.9 or >1.4), and no PAD. Clinical PAD was present in 150 patients (14.2%) and 298 cases of subclinical PAD were detected (28.3%). Patients with PAD (clinical and subclinical PAD) were significantly older and had a higher prevalence of hypertension and diabetes mellitus than those without PAD. During the 1-year follow-up, 59 patients died (5.6%). Previous PAD (hazard ratio 4.38, 95% confidence interval 1.96 to 9.82, p <0.001) and subclinical PAD (hazard ratio 2.35, 95% confidence interval 1.05 to 5.23, p <0.05) were associated with increased cardiovascular mortality. Moreover, patients with clinical PAD had higher rates of major cardiovascular events (myocardial infarction, angina, and heart failure) than patients with subclinical PAD or without PAD. In conclusion, beyond clinical PAD, measurement of ankle-brachial index after ACS provides substantial information on intermediate-term prognosis.

Prognostic value of low ankle–brachial index in patients with hypertension and acute coronary syndromes

Background Peripheral arterial disease (PAD) is associated with an increased risk of cardiovascular morbidity and mortality. Nevertheless, many patients are asymptomatic, and this condition frequently remains underdiagnosed. An ankle–brachial index (ABI) of less than 0.9 is a noninvasive and simple marker in the diagnosis of PAD and is also predictive of target organ damage in hypertension. The prognostic value of such measurements in hypertensive patients with acute coronary syndrome (ACS) is unknown. Methods The Prevalence of Peripheral Arterial Disease in Patients with Acute Coronary Syndrome registry is a multicentre, observational and prospective study that aims to describe the prevalence of and prognosis for PAD, diagnosed by ABI in hypertensive patients with ACS. Results One thousand one hundred and one hypertensive patients with ACS and at least 40 years of age were prospectively studied. Mean age of the population was 67.4 (11.4) years, and 67.7% were men. The prevalence of ABI less than 0.9 was 42.6% (469 patients). This subgroup was significantly older, had a higher prevalence of diabetes, previous coronary heart disease or stroke, left ventricular hypertrophy and more severe coronary lesions. Hospital mortality was higher in hypertensive patients with ABI less than 0.9 (2.3 vs. 0.2%; P < 0.01). An ABI less than 0.9 was associated with an increased risk of heart failure after ACS (odds ratio, 1.4; P = 0.04), higher hospital mortality (odds ratio, 13.0; P = 0.03) and the composite endpoint of mortality, heart failure and angina (odds ratio, 1.4; P = 0.03). Conclusion Asymptomatic PAD is highly prevalent in hypertensive patients with ACS. An ABI less than 0.9 identifies a subset of patients with more extensive target organ damage and higher risk of hospital cardiovascular complications after an ACS.

Coronary artery spasm and acute myocardial infarction in naproxen‐associated anaphylactic reaction

We present the case of a 43‐year‐old man who suffered an acute myocardial infarction after oral administration of 250 mg of naproxen, prescribed as antiinflammatory‐analgesic agent after tooth extraction. Both intradermal skin test and human basophil degranulation test were positive to naproxen. These findings suggest a naproxen‐associated anaphylactic reaction with concomitant coronary artery spasm and posteroinferior infarction, a clinical event previously not reported with the use of this drug.

Interatrial conduction block with retrograde activation of the left atrium and paroxysmal supraventricular tachyarrhythmias: influence of preventive antiarrhythmic treatment.

Patients with advanced interatrial conduction block with retrograde activation to the left atrium present a high incidence of supraventricular tachyarrhythmias. We report the value of preventive antiarrhythmic treatment in these patients.

Automatic measurement of corrected QT interval in Holter recordings: Comparison of its dynamic behavior in patients after myocardial infarction with and without life-threatening arrhythmias

This study was designed to determine the value of automatic corrected QT-interval measurement in Holter tapes in patients after myocardial infarction as a marker of life-threatening ventricular arrhythmias. We compared the corrected QT interval, automatically measured in 24-hour Holter recordings, in two groups of patients after myocardial infarction: group I was composed of 14 patients admitted consecutively to our hospital for documented sustained ventricular tachycardia or out-of-hospital cardiac arrest. Group II consisted of 28 patients with previous myocardial infarction with characteristics similar to those of group I, but without malignant ventricular arrhythmias in the follow-up. The global mean 24-hour corrected QT interval was longer in group I (425 +/- 20 msec) than in those patients after myocardial infarction without arrhythmias (group II) (405 +/- 17 msec; p < 0.01). Furthermore, a significant proportion of patients of group I (seven of 14) exhibited more peaks of corrected QT longer than 500 msec compared with patients of group II (two of 28; p < 0.005). A circadian rhythm of corrected QT peaks was observed in group I, having a significantly higher incidence from 11 PM to 11 AM (p < 0.05). We conclude that automatic corrected QT-interval measurement on Holter electrocardiogram is now available and feasible. Our results suggest that this is a marker for risk assessment of life-threatening ventricular arrhythmias. Large-scale trials are needed to confirm these results and to determine the predictive value of this technique for risk stratification.

Cardiac arrhythmias and left ventricular hypertrophy in systemic hypertension and their influences on prognosis

Left ventricular hypertrophy (LVH) is the adaptative mechanism of the heart to systolic overload of the left ventricle. Nevertheless, LVH plays a role in some complications, such as cardiac arrhythmias. Patients with LVH are more likely to develop ventricular arrhythmias than the hypertensive population without LVH. Further, the relation between left ventricular mass and ventricular arrhythmias is graded and continuous. The arrhythmias described in hypertensive patients with LVH are usually isolated premature ventricular contractions. The presence of electrocardiographic criteria of LVH represents a risk of higher incidence of sudden death, especially in men. The risk is even greater in the presence of ventricular arrhythmias. The presence of late potentials has been recently characterized as more related to ventricular arrhythmias than LVH. Antihypertensive drugs that can reduce LVH also have a beneficial effect on cardiovascular morbility and mortality.

Electrocardiographic and Clinical Precursors of Ventricular Fibrillation: Chain of Events

Precursors of VF. Ventricular fibrillation is the final event in the majority of cases of sudden death. The ECG and clinical precursors of ventricular fibrillation are discussed in this article. Ventricular fibrillation usually appears as a consequence of a chain of events that leads to the appearance of this lethal arrhythmia. We review the markers of the vulnerable myocardium prone to ventricular fibrillation, the triggers and modulators that act on this vulnerable myocardium, and the event(s) that constitute the final step preceding this arrhythmia. The final step may be as unique as a sudden waterfall or present as a cascade of successive phenomena.