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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. (C) 2012 Elsevier Inc. All rights reserved.

Eur J Clin Invest 2011; 41 (12): 1268–1274 Abstract Background Age is one the factors associated with poor prognosis in acute coronary syndromes (ACS) and elderly patients are a high-risk collective with few parameters for mid-term cardiovascular stratification. We aimed to assess the predictive value of ankle–brachial index (ABI) in patients (> 75 years) for 1-year mortality after an ACS. Materials and methods Prospective, observational and multicentre study of ACS patients in whom ABI was assessed during hospitalization. Results A total of 1·054 patients were included, mean age 66·6 (11·7) years from whom 26·6% were > 75 years. Elderly patients showed more history of cardiovascular disease and higher prevalence of all risk factors, except current smoking. Angiography and revascularization were performed less frequently in the elderly. Patients > 75 years showed higher presence of three vessel coronary disease and received fewer guideline-recommended treatments. Patients who died through the follow-up, mean time 387·9 ± 7·2 days, had lower ABI (0·73 ± 0·24 vs. 0·92 ± 0·22; P 75 years (HR: 2·30; IC 95% 1·26–4·18; P 0·90 and young patients with ABI

Introduction and objectives.The presence of peripheral arterial disease in patients with coronary artery disease is associated with a poor cardiovascular outcome. However, the majority of affected patients are asymptomatic and the condition is underdiagnosed. The ankle-brachial index (ABI) provides a simple method of diagnosis. The aim of this study was to assess the usefulness of an abnormal ABI for identifying multivessel coronary artery disease in patients with acute coronary syndrome (ACS). Methods. We analyzed data on all ACS patients included in the PAMISCA multicenter study (with 94 participating hospitals) who underwent catheterization during admission. Patients were diagnosed with multivessel coronary disease if two or more major epicardial vessels or the left main coronary artery, or both, were affected. An ABI ≤0.9 or >1.4 was considered abnormal. Results. The study included 1031 patients with a mean age of 67.7 years. Of these, 542 had multivessel disease (52.6%). Compared with those without multivessel disease, these patients were older (66.6 years vs 62.6 years; P

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 indexor=0.9 or1.4), 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, p0.001) and subclinical PAD (hazard ratio 2.35, 95% confidence interval 1.05 to 5.23, p0.05) 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.

ObjectiveA 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.MethodsThe PAMISCA register is a prospective, multicenter study involving patients ≥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.Results1410 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

New biological markers of myocardial injury have improved the management of patients with acute coronary syndromes. Among these markers, the most relevant are the cardiac troponins (troponin I and troponin T) because of their cardiospecificity, and myoglobin because of its combination of diagnostic sensitivity and usefulness for an early diagnosis. The serial analysis and combined use of both markers fulfill all diagnostic and prognostic requirements, and are helpful in indicating therapeutic strategies for acute coronary syndromes. However, these markers also have limitations, and their concentrations should always be interpreted in the light of the patient's clinical status.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in clinical practice. It is not a benign disease because is associated to a significant increase in mortality and morbidity. Thus, being AF a potentially dangerous arrhythmia, it seems logical to use antiarrhythmic strategies to avoid, or at least control, this rhythm disturbance [1, 2].

SummaryThe evidence of elevated levels of several biochemical markers of prothrombotic state in patients with unstable angina suggests that thrombus formation and lysis play a pivotal role in acute coronary syndromes. The clinical syndrome of unstable angina encompasses a variety of clinical presentations of transient episodes of myocardial ischemia. This study was designed to assess plasmin generation in different settings of unstable angina. Evidence of plasmin generation in patients with unstable angina was measured by circulating plasmin-α2 antiplas-min complexes (PAP). A second objective was to identify whether PAP levels had a prognostic value to predict outcome. Eighty-five patients admitted to the coronary care unit for unstable angina were classified into three groups. Group A included 26 patients with postinfarction angina; group B comprised 26 patients with new onset angina; and group C included 33 patients with crescendo angina. Mean PAP levels were higher in the three groups compared to healthy controls. A significant correlation was found between levels of PAP and D-dimer, particularly in postinfarction angina (r = 0.6; p Abbreviations and acronyms: CABG: coronary artery bypass graft; CCU: coronary care unit; ECG: electrocardiogram; IABP: intraaortic balloon pump; MI: myocardial infarction; PAP: plasmin-α2 antiplasmin complexes; PTCA: percutaneous transluminal coronary angioplasty

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; p0.01). 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; p0.005). A circadian rhythm of corrected QT peaks was observed in group I, having a significantly higher incidence from 11 PM to 11 AM (p0.05). 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.

The following images belong to a 86-year-old woman with severe aortic stenosis in whom a transcatheter aortic valve replacement (TAVR) was performed ([Figure 1][1], [Online Videos 1][2], [2][3], and [3][4]). Pre-procedural angiography revealed an anomalous origin of the left circumflex coronary

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.

Spontaneous coronary artery dissection is an unusual cause of acute coronary syndrome. We describe a series of cases that with an early diagnosis and aggressive treatment, which includes percutaneous angioplasty with stent implantation and cardiac surgery, had a good outcome. The objective was to study the demographic characteristics, clinical settings, treatments, and inhospital course of patients with spontaneous coronary artery dissection. We studied a retrospective case series in 3 coronary care units in third-level university hospitals. The spontaneous coronary artery dissection diagnosis was made by coronary angiography. Seven cases of spontaneous coronary artery dissections were recorded. They were 5 women and 2 men. The age range was 28 to 64 years. Two of them took oral contraceptives and one case occurred in the postpartum period. An acute anterior wall myocardial infarction was the most frequent clinical presentation, occurring in 4 of the 7 cases. In fact, the left anterior descending artery was involved in 6 cases. An urgent coronary angiogram was performed in all cases. Definitive treatment included percutaneous angioplasty and stent implantation in 3 cases, coronary artery bypass surgery in 2 case, and cardiac transplantation in another case. One patient was treated medically. None of the patients died in the hospital. Spontaneous coronary artery dissection remains an unusual cause of acute coronary syndrome. It should be included in the differential diagnosis of acute myocardial infarction, especially when it affects young, healthy females. An early clinical suspicion and diagnosis with urgent coronary angiography and aggressive treatment that includes percutaneous angioplasty with stent implantation and cardiac surgery could improve the prognosis of these patients.

The impact of target organ damage (TOD) clustering in hypertensive patients with established cardiovascular disease has not been clearly defined. Multicentre, observational and prospective study of 1054 consecutive patients with acute coronary syndromes (ACSs). The objective was describing the impact of TOD on first-year mortality. Ankle-brachial index (ABI), left ventricular hypertrophy and renal dysfunction were assessed during hospital stay. Hypertensive patients accounted for 80% of the cohort and had slightly higher mean age, higher prevalence of risk factors, previous cardiovascular disease and TOD. During follow-up, mean time 387.9 (7.2) days and median 382 (364.0-430.0) days, mortality rate tended to be higher in hypertensive patients (6.1 versus 3.5%; P = 0.16). Cox regression survival analysis identified pathological ABI as the only TOD independently associated with mortality. When assessed globally, the presence of at least one TOD predicted mortality only in patients with hypertension and differences in mortality rate appeared very early in the follow-up. A linear increase in mortality rate was observed with the clustering of TOD: 2.0%, if no TOD was present, 7.6% in one TOD, 11.1% in two TODs and 20.0%, if three TODs were present. An increased risk in the combined end point of ischaemic events was observed in hypertensive patients without TOD (odds ratio (OR): 3.18; 95% confidence interval (CI): 1.31-7.70; P = 0.01) and was still higher in patients with hypertension and TOD (OR: 4.61; 95% CI: 1.90-11.80; P < 0.01). TOD predicts mortality and ischaemic events of hypertensive patients after ACS. Journal of Human Hypertension (2011) 25, 600-607; doi:10.1038/jhh.2010.109; published online 16 December 2010

The relationship between silent myocardial ischemia and sudden death depends on the severity and duration of the ischemia. Severe, transmural and persistent ischemia, as occurs in myocardial infarction, can trigger sudden death. When the ischemia is severe and transmural but not long-standing (e.g., Prinzmetal angina), ventricular arrhythmias appear frequently, but they are rarely malignant. In cases of subendocardial ischemia, there is no definitive proof of this relationship.

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.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.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%; P0.01). 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).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.

The best therapeutic approach to the therapy of potentially malignant ventricular arrhythmias is still unknown, particularly in view of the increased mortality with flecainide and encainide shown in the CAST study. Various ongoing studies, particularly with amiodarone, will show whether better results can be obtained with other agents. Flecainide and encainide do, however, have a restricted place when other agents cannot be used. Low-dose amiodarone with low-dose flecainide may be worth trying.

Transient left ventricular apical ballooning (TAB) is a condition that mimics acute coronary syndrome typically without coronary angiographic stenosis. Patients present with typical chest pain, ECG changes suggesting ischemia, and a slight elevation of myocardial injury markers such as creatine kinase and troponines. Ballooning during ventricular systole of the cardiac apex is a characteristic feature of this entity. It is transient and it usually resolves after a few days together with normalization of ECG changes. Initially, apical dyskinesis can be diagnosed by any cardiac imaging technique that allows myocardial wall motion assessment. Recent advances in cardiovascular magnetic resonance imaging (CMR) have made this technique to become the gold-standard method to assess myocardial infarction. CMR provides an excellent and reproducible assessment of segmental wall motion abnormalities and, more importantly, it allows an accurate depiction of myocardial necrotic area by means of delayed contrast-enhancement method. Therefore, it may be particularly useful in the assessment of TAB by demonstrating segmental dysfunction in the absence of myocardial irreversible damage. We report three cases of TAB in which contrast- enhanced CMR emerged as an excellent diagnostic tool.

Primary ventricular fibrillation (VF) is an early complication of acute myocardial infarction (AMI), which was recently associated with high in-hospital mortality. 1 The usefulness of preventive antiarrhythmic drugs in patients with symptoms of acute coronary ischemia has been addressed in different studies, 2,3 but less attention has been given to the identification of AMI patients with a high risk for VF. Admission data for predicting VF in AMI have been assessed by Flugelman et al 4–5 and Molstad 6 using multiple logistic regression formulas. In the first study, however, ventricular tachycardia was included as the end point for analysis, and no distinction was made between primary and secondary VF, whereas in the second study, only variables of doubtful value in clinical practice were considered. We investigated the usefulness of routine clinical, electrocardiographic and laboratory parameters for predicting the development of VF in patients with AMI in Killip's functional class I and II.

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.

Background Chest pain is a frequent symptom in the emergency department and often presents a diagnostic challenge. Because coronary thrombosis is a hallmark of acute ischemic syndromes, the substrates of the coagulation and fibrinolysis cascades may be markers of coronary ischemia. The objective of this study was to determine the diagnostic value of several hemostatic markers in patients presenting to the emergency department (ED) with chest pain syndromes. Methods Two hundred fifty-seven consecutive patients with acute chest pain were studied in this prospective study conducted in an urban ED. D- Dimer levels were measured at admission to the ED in all patients. We also measured thrombin-antithrombin complexes, prothrombin fragment 1+2, activated factor VII, and fibrinogen. We used regression analysis to estimate the likelihood of myocardial infarction and the diagnostic value of D -dimer. Results D -Dimer and fibrinogen levels were significantly higher in patients with acute ischemic events (myocardial infarction and unstable angina) than in nonischemic patients ( P P =.02, respectively). The other hemostatic markers were not significantly elevated in patients with ischemic events. D -Dimer level >500 μg/L had an independent diagnostic value for myocardial infarction and increased the diagnostic sensitivity of the electrocardiogram and history from 73% to 92%. Conclusion D -Dimer, an expression of ongoing thrombus formation and lysis, is a marker of substantial incremental value for the early diagnosis of acute coronary syndromes presenting with chest pain. It adds independent information to the traditional assessment for myocardial infarction. D -Dimer can be incorporated into clinical decision models in the ED. (Am Heart J 2000;140:379-84.)

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.

The problem of risk stratification after myocardial infarction is reviewed. There are three major complications: new ischemic events, congestive heart failure, and malignant arrhythmias and sudden death, related to the presence of residual ischemia, left ventricular dysfunction, and electrical instability. The bidirectional interactions among these three factors is analyzed. The risk is in the middle of a triangle, the three angles of which are the above-mentioned factors. All the “satellite” factors that appear from all three angles are presented. Furthermore, the most important parameters and techniques employed to detect risk, multifactorial approach of risk stratification, and changes of risk stratification in the thrombolytic era are briefly reviewed.

There is conclusive experimental and clinical evidence that severe, transmural and persistent acute ischemia (silent or symptomatic), the maximum exponent of which is myocardial infarction, can trigger malignant ventricular arrhythmias and sudden cardiac death. 1 Furthermore, a relation between severe acute transmural but transient ischemia appearing during Prinzmetal's angina 2 or during percutaneous transluminal angioplasty 3 and ventricular arrhythmias is well known, although such arrhythmias are rarely malignant. However, the relation between ventricular arrhythmias and subendocardial ischemia (silent or symptomatic) has only been partially studied, and results are contradictory. 4–7

We describe the criteria for differential diagnosis between 3:2 sinoatrial block from atrial bigeminy due to an ectopic focus in the sinus or parasinus zone. In the 3:2 sinoatrial block the RR interval of the basic rhythm is similar to the short R-R interval of the paired rhythm. In atrial bigeminy, the R-R interval of the basic rhythm is similar to the long R-R interval of the paired rhythm. (Chest 1991; 99:735–36)

EDITOR—Spirito and Autore recommend β blockers or verapamil, or the two drugs combined, to control heart rate in patients with hypertrophic cardiomyopathy and chronic atrial fibrillation. To recommend the combination …

The Poincare plots-a simple graphical, nonlinear method was implemented to express 24-h QT interval changes. The group of 23 pts with hypertrophic cardiomyopathy was analyzed (11 pts. with higher and 12 with lower risk of sudden cardiac death). The control group consisted of 10 healthy subjects. 24-h Holter ECG recordings were analyzed and RR and QT intervals were measured beat by beat. 3 dimensional QT and RR plots were constructed in the time delay coordinates. Three main forms of QT plots were observed, highly different in cases with hypertrophic cardiomyopathy compared to normals. Different shapes of QT and RR plots revealed a complex nonlinear relation of the QT and RR intervals.

Excerpt To the editor: Drug-induced lupus erythematosus is characterized by a wide spectrum of clinical symptoms, ranging from mild arthralgias to systemic involvement, although photosensitivity an...