As a consequence of successful, large-scale primary prevention strategies, the incidence, and prevalence of atherosclerotic diseases continuously have reduced over the last two to three decades [9], and we can consider this secular epidemics nearly eradicated, as it happened with previous centuries’ plagues, syphilis, and tuberculosis, each within its own reference century. As a consequence, atherosclerotic diseases occur less and later in life, and with the shortening of the “vascular” causes of heart disease, those due to aging-associated tissue degeneration, come forward.

Numerous cellular mechanisms underlie the aging of the cardiovascular system, including replicative senescence, apoptosis, protein misfolding, and low-grade inflammation [10]. Typical aging-associated anatomical modifications are represented by increased left ventricular mass, left atrial size, myocardial collagen deposition, and calcium deposition in valvular structures and coronary arteries. Large arteries are stiffened due to collagen overproduction, calcification, and endothelial dysfunction. Isolated systolic hypertension, calcific aortic stenosis, and senile cardiac amyloidosis are frequent hallmarks of the degenerative processes, along with increased prevalence of multivessel, calcific coronary atherosclerosis. All these factors contribute to explain the increasing prevalence of heart failure with preserved left ventricular ejection fraction and diastolic dysfunction, which is not linked to necrotic tissue loss secondary to coronary artery disease but rather to progressive replacement by fibrotic tissue. The same holds true for atrial fibrillation, which presents in up to 15 % of individuals above 80 years of age and is linked to degeneration of atrial tissue and to atrial enlargement secondary to ventricular diastolic dysfunction. Therefore, the present epidemiological picture is characterized by an increasing prevalence of non ST segment elevation myocardial infarction, chronic heart failure, and atrial fibrillation, all occurring in an increasingly aged population presenting with multiple problems at the level of other organs and systems.

Multimorbidity (≥2 concurrent diseases) is present in the overwhelming majority of older adults and increases the likelihood of many adverse outcomes, such as hospital readmission, disability, and death [11]. Chronic kidney disease [12] and cancer are conditions to be often taken into account in many clinical scenarios, for example, because acutely worsening renal insufficiency may be precipitated by contrast medium used for coronary angiography or because reduced life expectancy due to cancer may exclude otherwise indicated interventions. Since evidence-based medicine has been built on results gathered in younger or middle-aged population, the commonly used guidelines are of limited utility. In older adults with multimorbidity, patient’s preferences, prognosis, clinical feasibility, and reasonably optimized therapies are to be taken first into account in the decision-making process, interpreting the evidence on an individual basis.

Despite this, the high cardiovascular morbidity and mortality of the elderly should deserve an aggressive and technologically advanced treatment, whenever possible. Despite trials have reported that the complication rate from early invasive procedures for acute coronary syndromes is substantially higher in patients older than 75 years [13], in registry studies [14–16] and in observational studies, aggressive treatment proved even more effective in terms of reduced number needed to treat, compared to younger adults [14]. Nonetheless, as already mentioned, registry studies report that older patients are systematically undertreated in parallel with their increasing burden of comorbidities [7]. Similar findings, which introduce the concept of a “net clinical benefit” that may increase with increasing age, has been found in other clinical areas, such as anticoagulation to prevent cardioembolic stroke in atrial fibrillation [17], where older patients are again systematically undertreated.

Cognitive impairment including deficits in memory and executive function is, among several geriatric syndromes, one of the most frequent comorbidities [18–22], with a well-established relationship with poor outcomes in several cardiovascular conditions such as chronic heart failure [3]. Urinary incontinence (18–45 %), falls (32–43 %), and frailty (14–25 %) are other geriatric syndromes with high prevalence that commonly complicate the management of chronic heart failure in older adults [23].

Frailty, generally defined as a reduced homeostatic reserve leading to increased vulnerability to stressors, has gained attention in recent years as another geriatric syndrome associated with adverse health outcomes [24–26]. Frailty must be taken into account in clinical decision-making in elective procedures very commonly indicated in geriatric cardiac patients. For example, instruments for risk assessment in candidates to elective cardiac surgery or interventional procedures (e.g., transcatheter aortic valve implantation, TAVI), which have been built from data collected in middle-aged or young-adult populations, are inaccurately predictive when applied to older patients, and this has prompted an increasing research interest in testing the clinical utility of frailty indexes in improving the prediction of risk [27]. In the original PARTNER randomized trial, 31 % of patients died within 1 year even after immediately successful aortic valve replacement [28], an observation that underlines the need for improved identification of those older patients who might really profit long-term from TAVI. Following PARTNER, frailty has been identified as a syndrome that meaningfully predicts outcomes in older adult candidates to TAVI [29, 30].