Atrial fibrillation (AF) and heart failure (HF) are evaluated here together because pathophysiological/hemodynamic factors in these two conditions interact when AF and HF coexist. A more comprehensive coverage of AF and other supraventricular dysrhythmias can be found in many other sources (including Rautaharju and Rautaharju [1]).

The evolution of hypertensive heart disease and development of left ventricular hypertrophy (LVH) play an important role in the mechanism for HF. These aspects are covered in Chap.​ 7. The importance of left bundle branch block (LBBB) as a predictor of HF is covered in Chap.​ 8. Although AF is not a short-terms causal factor for acute fatal events, identification of predictors of AF is still an important area of cardiac research. Preventing AF would have a more important impact on public health than attempts to prevent adverse cardiovascular (CVD) events after AF occurs. The relatively high prevalence of AF and the associated impaired quality of life particularly in older women signifies the importance of this condition and its prevention. From various supraventricular arrhythmias only atrial fibrillation will be considered here.

The quality of life of women with AF is more impaired than in men. In the Canadian Trial of Atrial Fibrillation the quality of life was evaluated at baseline, 3 and 6 months after antiarrhythmic drug treatment [2]. At the baseline the reported physical health and functional capacity in women after controlling for clinical and demographic factors was worse compared to those reported by men but there was no significant gender difference in reported mental health or general well-being. Women also had significantly more frequent and more severe cardiac symptoms than men. Physical health improved significantly from baseline to 3 months in women but not in men and conversely, mental health improved for men but not for women p<0.001 for all. Cardiac symptom frequency and severity improved over time for women and men. Gender difference in the reported quality of life is in part due to the tendency in women to somatize, i.e., to amplify bodily sensations but the gender difference in quality of life remained significant after controlling for somatization. Women with AF have a high risk of stroke, in women older than 75 years particularly embolic stroke [3]. AF treatment in women has been found more conservative with less rhythm control than in men and intervention is more commonly delayed in women [4] although restoration of sinus rhythm with electrical cardioversion has been found equally successful in women than in men [2].

AF is generally a manifestation of evolving subclinical CVD or has already clinically manifest CVD. Of the 141 women with AF in the 1994 report from CHS referred to above [5], 54 % had a clinical CVD and another 40 % had subclinical CVD. Clinical CVD diagnosis included a history of myocardial infarction (MI), silent ECG-MI, history of angina pectoris, stroke, transient ischemic attack (TIA), congestive heart failure, rheumatic heart disease, intermittent claudication, history of coronary artery bypass graft operation, percutaneous coronary artery angioplasty, carotid endarterectomy, and angioplasty or bypass surgery of arteries in leg. Three subsets of conditions defined subclinical CVD: (1) subclinical atrial/valvular disease (abnormal mitral or aortic valve function or abnormal left atrial dimension on M-mode echocardiogram); (2) subclinical ventricular disease (abnormal left ventricular wall motion of ejection fraction on echocardiogram or abnormal left ventricular mass (≥192.3 g in women and 256.3 g in men; 80th percentile by gender); and (3) subclinical atherosclerotic disease (ultrasound-defined carotid stenosis (≥25 % on either side), ankle-arm index <0.9, or gender-specific common or internal carotid artery mean intimal-medial thickness above 8th percentile.

Significant correlates of AF were evaluated in CHS by Furberg et al. [5]. Logistic regression was used to estimate odds ratios for the association between AF and various risk factors, clinical and subclinical diseases. In this sequential selection procedure factors with significant univariate correlation with AF the factors with significant correlation with AF in the final multivariate model were called ‘correlators’. The following significant correlators were identified: (a) from clinical factors congestive heart failure and rheumatic heart disease; (b) from subclinical factors mitral stenosis, left atrial dimension and aortic regurgitation; and (c), from CVD risk factors, only treated hypertension remained a significant AF correlator. This sequential stepwise selection scheme excluded the following factors which were significantly associated with AF as single factors: (a) from clinical factors myocardial infarction and angina; (b) from subclinical factors abnormal ejection fraction, abnormal wall motion and left ventricular mass; and (c) from HF risk factors diabetes and serum glucose.

The results from this CHS report demonstrated that most elderly persons with AF have clinically confirmed CVD and that AF patients without clinically manifest CVD had subclinical CVD. Thus, lone AF is rare in elderly persons. A careful history and physical examination are the cornerstones in identification of clinical CVD. Echocardiograhic and other imaging procedures will effectively identify subclinical CVD. Consideration of these diagnostic procedures seems warranted in patients with AF. AF by self-report may be less accurate although careful consideration of prescribed medication use will increase the confidence in AF by self-report. Also, consideration should be given to the fact that AF is often transient as shown by ambulatory 24-h recordings [6].

In a 1997 report from the ARIC population [7] incident AF was strongly associated with age and its prevalence was lower in women than in men (10.1 and 21.6 per 1,000 person-years in women 65–74 and 75–84 years, respectively, and in men 17.6 and 42.7, respectively). Among other factors diuretic use, valvular heart disease and CHD, systolic blood pressure, glucose and left atrial size were associated with increased risk of AF in stepwise models. In their conclusions the authors emphasized the importance of left atrial size as an important risk factor for incident AF and potential importance of blood pressure control and glucose in preventing the development of AF.

Pathophysiological and functional interactions involved in the relationships between AF and HF are complex and there are conceptual problems in evaluation and interpreting clinical and ECG correlates and predictors of AF and HF. The block diagram in Fig. 5.1 shows the pathways of evolution from a CVD-free status to a condition where HF and AF are combined forming the vicious circle as noted above. Concerning AF and HF, the question remains which condition is the cause and which is the consequence. Impaired hemodynamics in AF includes high heart rate, reduced LV filling time and cardiac output. Loss of effective atrial contraction is detrimental particularly in patients with diastolic HF. In patients with HF and normal sinus rhythm the onset of new AF worsens cardiac function, peak oxygen consumption and mitral and aortic regurgitation [8]. Age, hypertension and diabetes as well as conditions precipitating structural myocardial abnormalities are common risk factors for AF and HF and the associated electrophysiological and neurohormonal alterations create a vicious circle whereby AF and HF further aggravate each other [9].