Cardiovascular diseases and neoplasms are closely interconnected, as each can stimulate or accelerate the development of the other. In particular, anticancer therapies that have significantly improved patient survival have also proven to be toxic—not only to the heart but to the entire cardiovascular system. It is therefore crucial to assess the risk of cardiotoxicity and to guide the patient throughout the entire course of treatment. In this context, the preparation of an accurate cardio-oncologic report is of paramount importance, as it facilitates the feasibility and safety of chemotherapy while minimizing the risk of preventable cardiovascular complications.

Cardiovascular Diseases and Cancer

Cancer and cardiovascular diseases are closely interconnected. From an epidemiological standpoint, they account for approximately two-thirds of all deaths in industrialized countries (Italy is no exception, as 7 out of 10 deaths are due to cardiovascular diseases or cancer) [1]. These conditions share common risk factors—such as smoking, obesity, physical inactivity, type 2 diabetes, and alcohol abuse—and are underpinned by similar pathophysiological mechanisms, particularly chronic inflammation, which may ultimately lead to the development of malignant tumors or overt cardiovascular disease.

It has been demonstrated that cancer itself can promote the progression of cardiovascular disease—not only ischemic heart disease, but also arterial and venous thromboembolic events, various types of arrhythmias, peripheral artery disease, and ventricular dysfunction [2,3].

Oncologic therapies, which have greatly improved the prognosis of cancer patients, may nevertheless prove toxic not only to the heart but to the entire cardiovascular system (see Figure 1 and Table 1 below) [4].

Table 1. Cardiovascular complications of anticancer therapies.

The Damaged Heart

A damaged heart—either infarcted or failing—releases pro-oncogenic cardiokines, such as SerpinA3, into the cardiac stroma [5]. In addition, tissue hypoxia triggers the expression of vascular growth factors and promotes neoangiogenesis [6].

Patients affected by cardiovascular diseases typically undergo medical follow-ups more frequently than the general population. These evaluations can often lead to an earlier diagnosis of cancer (for example, a pulmonary nodule identified on chest X-ray or CT scan). Furthermore, certain therapies prescribed for specific cardiovascular conditions may incidentally reveal an occult malignancy—for instance, anticoagulant therapy administered for cardioembolic prevention in patients with atrial fibrillation may unmask gastrointestinal bleeding, which in some cases can conceal an underlying gastrointestinal cancer.

Some types of cardiac tumors are associated with genetic disorders, highlighting the role of genetic predisposition in certain conditions—for example, tuberous sclerosis, an autosomal dominant disease often associated with cardiac rhabdomyoma.

Inflammation generated by atherosclerosis may accelerate cancer progression, while thrombin produced in thrombotic processes can promote metastasis and inflammation. Clonal hematopoiesis of indeterminate potential (CHIP) may also represent a shared upstream mechanism underlying both diseases: aging-related accumulation of somatic mutations in hematopoietic stem cells leads to clonal expansion, which can result not only in leukemia but also in atherosclerotic coronary heart disease (CHD) [7].

We are facing a true pandemic of cardio-oncologic patients. In Italy, approximately 3% of the population are cancer survivors—an estimated 3.5 million long-term survivors—whose numbers and average age will continue to increase thanks to remarkable advances in oncology.

However, these same patients are likely to develop cardiovascular diseases for all the aforementioned reasons.

To provide a tangible framework for understanding these mechanisms, a classification of cardio-oncologic syndromes has been developed (see Figure 2).

There is, therefore, a need to work within a team of qualified professionals who can take into account all the aspects discussed here, accompanying the patient throughout the entire course of treatment. The goal is not to deny access to life-saving anticancer therapies, but rather to establish protocols that allow patients to be treated safely.

It is thus essential that the cardiologist assesses the risk of developing cardiovascular toxicity associated with anticancer therapy. This is a dynamic variable that depends on several factors (see Table 2) and must be periodically reassessed over time. Intuitively, the higher the risk of cardiotoxicity, the more frequent the follow-up visits should be, with early initiation of cardioprotective therapy when appropriate.

Table 2. Factors associated with cardiovascular toxicity secondary to anticancer therapies.

Abbreviation notes

• CTR-CVT: Cancer Therapy–Related Cardiovascular Toxicity
• BNP/NT-proBNP: B-type Natriuretic Peptide / N-terminal pro-B-type Natriuretic Peptide
• Tn: Troponin
• CVRFs: Cardiovascular Risk Factors
• ECG: Electrocardiogram
• ETT: Exercise Tolerance Test (Stress Echocardiography)
• eGFR: Estimated Glomerular Filtration Rate

The Cardio-Oncologic Report

The term report (from the Latin refertum, meaning “to convey information”) refers to the structured communication between the cardiologist, the oncologist/hematologist, and the general practitioner.

The cardio-oncologic report must include a thorough past and recent medical history, documenting the presence of any cardiovascular disease (previous or current), cardiovascular risk factors (which largely overlap with those for many types of cancer), and specific risk factors for therapy-related cardiovascular toxicity. These latter include a prior history of cancer, type and cumulative dose of anticancer agents used, any previous exposure to chemotherapy and/or radiotherapy, and current treatment protocols.

Laboratory testing should include cardiac troponin and NT-proBNP, the former being a marker of myocardial cellular injury and the latter reflecting the patient’s hemodynamic status. Standard laboratory analyses should also comprise a complete blood count, renal, hepatic, lipid, and coagulation profiles, urinalysis, and electrolyte levels. Depletion of calcium, potassium, or magnesium may contribute to QT interval 

prolongation—particularly relevant in patients who, as a reactive response to cancer diagnosis, may develop depressive syndromes and be treated with antidepressants known to lengthen the QT interval, thereby predisposing to malignant arrhythmias such as torsades de pointes, which may rapidly degenerate into ventricular fibrillation.

Guidelines recommend correcting the QT interval for heart rate using Fridericia’s formula, which provides a more reliable adjustment at higher heart rates—a common condition in cancer patients with sinus tachycardia due to anemia, anxiety, or fever.

Particular attention should be paid to patient-reported symptoms such as angina or heart failure manifestations, palpitations, and presyncopal or syncopal episodes, which may represent evidence of underlying cardiac pathology but can also reflect the primary oncologic disease. Assessing functional capacity provides an objective indication of the patient’s overall clinical condition.

The echocardiographic report must be comprehensive and annexed to the overall cardio-oncologic report. A concise summary may be included in the main report, describing left ventricular geometry, systolic function (including biplane ejection fraction by modified Simpson’s method and global longitudinal strain, GLS). A relative reduction in GLS of 15% from baseline indicates early subclinical left ventricular dysfunction related to anticancer

therapy—an important prognostic finding that precedes detectable ejection fraction decline. The report should also address filling pressures and any valvular or pericardial abnormalities.

Cardiovascular risk must always be estimated using the SCORE2 or SCORE2- OP algorithms, while risk of therapy-related cardiovascular toxicity should be quantified using the ICOS risk score. The latter varies according to the anticancer strategy adopted.

According to the European cardio-oncology guidelines⁸, available calculators (also as smartphone applications) integrate all relevant clinical parameters to categorize patients into low, intermediate, high, or very high-risk groups. Each category corresponds to specific recommendations for monitoring frequency and follow-up scheduling (see Figure 3).

These data should always be included in the cardio-oncologic report, ensuring that oncologists, hematologists, and general practitioners have full access to all relevant cardiovascular information.

Abbreviation notes

• ECG: Electrocardiogram
• ETT: Echocardiography (Transthoracic Echocardiogram)
• cTn: Cardiac Troponin
• NT-proBNP: N-terminal pro–B-type Natriuretic Peptide
• C1–C6: Chemotherapy cycles 1 through 6
• Post tx: After completion of therapy
• 3M / 12M: Three- and twelve-months post therapy
• ESC Class I / IIa / IIb: Strength of recommendation per European Society of Cardiology guidelines

The number of long-term cancer survivors is steadily increasing, and a considerable proportion of these patients will likely develop cardiovascular diseases. More than ever, there is a pressing need to establish structured and standardized diagnostic and therapeutic pathways for these individuals.

In this context, the cardio-oncologic report represents a powerful tool to ensure the most accurate and comprehensive description of all the clinical elements required to guarantee patient safety, while allowing access to life-saving oncologic therapies without undue restriction.

The risk of developing cancer therapy–related cardiovascular toxicity (CTR-CVT) should always be carefully assessed and monitored:

a) Routine evaluation should include blood pressure, heart rate, height, body weight, and body mass index (BMI).

b) When feasible, cardiac biomarkers (troponin and natriuretic peptides) should be measured in patients at risk of CTR-CVT; results must be interpreted according to the patient’s clinical condition, type of anticancer therapy, and renal function.

c) In selected patients, additional complementary cardiovascular imaging or functional tests — such as cardiac magnetic resonance (CMR), coronary computed tomography angiography (CCTA), or cardiopulmonary exercise testing (CPET) — should be considered.