Reversible congestive heart failure associated with diabetes mellitus in two cats

Abstract

Case series summary

This report describes two cats diagnosed with diabetes mellitus who developed clinical signs consistent with congestive heart failure (CHF). Clinical and echocardiographic findings improved over time with stabilisation and optimisation of glycaemic management. Both cats presented with dyspnoea, hypotension and hypothermia. Thoracic radiographs demonstrated diffuse pulmonary infiltrates. Pleural effusion was identified in one case. Echocardiography revealed left ventricular thickening with left atrial enlargement. Laboratory abnormalities included hyperglycaemia, elevated fructosamine and increased N-terminal pro B-type natriuretic peptide (NT-proBNP) concentrations. After CHF therapy and insulin administration, both cats showed rapid clinical improvement, with NT-proBNP concentrations decreasing into the reference interval and improvement in echocardiographic parameters within weeks. One cat later again showed an increase in myocardial thickness and experienced recurrence of CHF during a period of poor glycaemic control, with subsequent improvement after intensified glycaemic management.

Relevance and novel information

To the authors’ knowledge, this is the first report describing cats diagnosed with diabetes mellitus who developed CHF accompanied by increased left ventricular wall thickness and left atrial enlargement on echocardiography, with subsequent improvement after clinical stabilisation and glycaemic management. These cases suggest a potential association between metabolic dysregulation and the occurrence of CHF in cats.

Plain language summary

Two cats with diabetes developed reversible heart failure

This report describes two cats with diabetes mellitus who developed signs of heart failure, including breathing difficulties and fluid accumulation in the lungs or chest. Heart scans showed thickening of the heart muscle and enlargement of the left atrium. After treatment for heart failure and careful control of blood glucose levels with insulin, both cats improved quickly. Their breathing returned to normal, and heart abnormalities became less severe over time. Blood markers associated with heart disease also returned to normal levels. In one cat, heart failure returned when blood glucose was not well controlled but improved again after treatment was restarted. These findings suggest that poor control of diabetes may affect heart function in cats and, in some cases, lead to heart failure. Importantly, this type of heart problem may be reversible with appropriate treatment. Early recognition and proper management of diabetes may help prevent or reduce heart complications in affected cats.

Keywords

Congestive heart failure diabetes mellitus echocardiography glycaemic management

Introduction

Diabetes mellitus (DM) is a common endocrine disorder in cats, associated with metabolic dysregulation, insulin deficiency or resistance, and systemic complications.¹

Reversible forms of cardiomyopathy are increasingly recognised in cats, with transient myocardial thickening (TMT) describing a pattern of temporary left ventricular (LV) wall thickening that may be accompanied by congestive heart failure (CHF).^2
–5 Several endocrine disorders have been reported to induce reversible myocardial remodelling and CHF in cats.^6
–8 As DM is a systemic metabolic disorder, it may also influence cardiac structure and function; however, its association with reversible myocardial changes and CHF in cats remains unclear.

Here, we describe two cats with poorly controlled DM who developed CHF with LV wall thickening and left atrial (LA) enlargement on echocardiography, followed by improvement after clinical stabilisation and optimisation of glycaemic control. To the authors’ knowledge, this presentation has not previously been reported in cats.

Case series description

Case 1

An 8-year-old, 4.0 kg, spayed female British Shorthair cat was referred for acute dyspnoea, with no prior fluid therapy. The cat had been diagnosed with DM at another veterinary hospital 1 month earlier and had not yet received insulin therapy; polyuria and polydipsia had worsened in the days before presentation.

Physical examination revealed hypothermia (36.6°C), tachypnoea (64 breaths/min), hypotension (systolic blood pressure [SBP] 90 mmHg; reference interval [RI] 110–130)⁹ and a heart rate of 147 beats/min. The cat also had mildly tacky mucous membranes and a slightly prolonged skin tent, findings suggestive of mild dehydration.

Blood tests showed marked hyperglycaemia (359 mg/dl; RI 71–148), elevated fructosamine (416 µmol/l; RI 154–331)¹⁰ and increased NT-proBNP (>1500 pmol/l; RI <100)¹¹ (Table 1), with elevated blood urea nitrogen (BUN) (83 mg/dl); other parameters were within RIs (Table 2). Urinalysis showed marked glucosuria (4+ on urine dipstick) without ketonuria.

Table 1

Serial echocardiographic and cardiac biomarker measurements in two diabetic cats with reversible congestive heart failure

	Case 1					Case 2
Parameter	Day 0	Day 7 (discharge)	Day 13	Day 34	Day 190	Day 0	Day 8 (discharge)	Day 17	Day 135 (relapse)	Day 180
IVSd (mm)	7.3	7.2	5.5	4.7	4.6	8.5	7.8	5.8	6.3	5.8
LVFWd (mm)	6.4	6.5	4.7	4.2	4.4	7.5	5.8	4	5.3	5.2
LA:Ao	2.19	2.2	1.42	1.65	1.47	1.8	1.8	1.5	2.4	1.36
LA FS (%)	7.6	7.8	25.5	–	34	8.5	22	29	16	32
LAD (mm)	18.4	18.7	12.6	14.5	14.6	16.7	17	13.5	22	12.6
LVIDd (mm)	9.4	10.7	–	11.7	12	10.2	13.6	–	11.3	14.4
LVIDs (mm)	6.1	6.4	–	7.1	8	4.1	8.3	–	4.7	3.6
NT-proBNP (pmol/l)	>1500	–	<50	–	–	1367	–	–	–	<50

IVSd = interventricular septal thickness in diastole; LA:Ao = left atrium:aorta ratio (right parasternal short-axis view); LA FS = left atrial fractional shortening; LAD = left atrial diameter (right parasternal long-axis four-chamber view); LVFWd = left ventricular free wall thickness in diastole; LVIDd = left ventricular internal diameter in diastole; LVIDs = left ventricular internal diameter in systole; NT-proBNP = N-terminal pro-B-type natriuretic peptide

Table 2

Serial haematological and biochemical findings in two diabetic cats with reversible congestive heart failure

Parameter	Case 1				Case 2					RI
Parameter	Day 0	Day 7 (discharge)	Day 13	Day 34	Day 0	Day 8 (discharge)	Day 17	Day 135 (relapse)	Day 180	RI
Glucose (mg/dl)	359	235	185	109	625	279	146	431	137	71–148
Fructosamine (µmol/l)	416	–	–	–	365	–	212	558	331	154–331
HCT (%)	38	–	–	–	47	–	–	57	55	30–52
WBCs (K/µl)	7.1	–	–	–	6.3	–	–	9.0	7.0	2.8–17
Neutrophils (K/µl)	5.8	–	–	–	4.9	–	–	6	4.5	2.3–10.3
Neutrophils (%)	82	–	–	–	77	–	–	67	64	–
Total protein (g/dl)	6.8	–	–	–	7.1	8	–	–	–	5.7–7.8
Albumin (g/dl)	3.4	–	–	–	2.5	3.2	–	–	–	2.3–3.5
BUN (mg/dl)	83	47	57	31	42	–	30	25	28	18–33
Creatinine (mg/dl)	1.6	2.3	2.6	1.8	1.4	–	1.2	0.9	1.1	0.8–1.6
Phosphate (mg/dl)	4.3	6	4.6	3.3	4.3	–	3.2	5.2	3.5	3.0–6.0
T4 (µg/dl)	1.2	–	–	–	1	–	1.8	–	–	0.8–4.7
Ketone (mmol/l)	0.2	–	–	–	0.2	–	–	0.1	–	0.0–0.3
Sodium (mEq/l)	150	151	149	162	152	149	157	151	153	145–158
Potassium (mEq/l)	4	4.5	2.5	3.7	4	3.7	3.7	3.8	4.5	3.5–5.1
Chloride (mEq/l)	108	110	105	127	112	117	117	114	118	112–129
Ionised calcium (mmol/l)	1.19	1.26	1.27	1.36	1.26	1.37	1.37	1.21	1.23	1.17–1.35

BUN = blood urea nitrogen; HCT = haematocrit; RI = reference interval; T4 = total thyroxine; WBCs = white blood cells

Thoracic radiographs showed diffuse pulmonary infiltrates compatible with cardiogenic pulmonary oedema. Echocardiography revealed asymmetric LV wall thickening at end-diastole, predominantly involving the interventricular septum (IVSd; 7.3 mm; RI <6), with concurrent thickening of the left ventricular free wall (LVFWd; 6.4 mm).^12,13 LA enlargement (left atrium:aorta [LA:Ao] ratio 2.19; RI <1.5)^13,14 and reduced LA fractional shortening (7.6%; RI 26 ± 10).^15,16 The left ventricular internal diameter in diastole (LVIDd) was reduced at 9.4 mm (RI for a 4 kg cat 12.2–19.2), while the left ventricular internal diameter in systole (LVIDs) was 6.1 mm (RI 5.5–12.6).¹³ No LV outflow tract obstruction was detected (Table 1).

Treatment included oxygen supplementation, furosemide (1 mg/kg IV q8h), pimobendan (0.25 mg/kg PO q12h), clopidogrel (18.75 mg/cat PO q24h) and a continuous rate infusion (CRI) of dobutamine (2.5 µg/kg/min). At presentation, the cat showed signs of a low cardiac output state, prompting inotropic support with dobutamine. After initiation of therapy, respiratory distress improved, thoracic radiographs demonstrated improvement in pulmonary infiltrates and blood pressure improved on physical examination. Glycaemic control was initially achieved with regular insulin (1 U IM q12h), which was subsequently transitioned to glargine (0.5 U SC q12h). The cat stabilised and was discharged after a 7-day hospitalisation on oral furosemide (1 mg/kg q12h), pimobendan (0.25 mg/kg q12h), clopidogrel (18.75 mg/cat q24h) and glargine insulin (0.5 U SC q12h). At discharge, IVSd remained increased (7.2 mm) and LVIDd remained below the RI (10.7 mm) (Table 1).

By day 13, the cat was clinically stable, with resolution of respiratory signs and improved respiratory rate, body temperature and blood pressure on physical examination. IVSd had decreased from 7.3 mm to 5.5 mm, LA:Ao from 2.19 to 1.42, and LA fractional shortening had improved from 7.6% to 25.5% (Table 1). NT-proBNP fell from above 1500 pmol/l to below 50 pmol/l, and blood glucose to 185 mg/dl (Table 2). By day 34, IVSd had further decreased to 4.7 mm and LA:Ao to 1.65, with blood glucose at 109 mg/dl. Representative echocardiographic images are shown in Figure 1. The cat remained clinically stable without recurrence of respiratory signs. Cardiac medications were discontinued within 4 weeks after marked improvement in echocardiographic findings and diabetic remission subsequently allowed cessation of insulin therapy. More than 6 months after withdrawal of all treatments, no recurrence of hyperglycaemia or CHF was observed, with serial echocardiography showing no further progression of cardiac structural changes (Table 1).

Figure 1

Echocardiographic images from case 1. (a) Short-axis view at the papillary muscle level at end-diastole and (b) the right parasternal short-axis view at the level of the aortic root at end-systole at the initial presentation, demonstrating left atrial enlargement and left ventricular hypertrophy. (c,d) The same views obtained 34 days later show reduction in left atrial size and left ventricular wall thickness, consistent with improvement in cardiac remodelling

Case 2

A 12-year-old, 6 kg, castrated male Korean Shorthair cat presented with acute respiratory distress and lethargy. The cat had been diagnosed with DM at another veterinary hospital 2 months earlier but had not yet received insulin therapy before presentation, with worsening polyuria and polydipsia. No prior fluid therapy had been administered. On admission, the cat was hypothermic (36.9°C), hypotensive (SBP 70 mmHg), tachypnoeic (60 breaths/min), with a heart rate of 160 beats/min, bilateral crackles and mild dehydration.

Blood tests showed marked hyperglycaemia (625 mg/dl), elevated fructosamine (365 µmol/l) and NT-proBNP (1367 pmol/l), with mild elevation of BUN; other parameters were within RIs (Table 2). Urinalysis showed marked glucosuria without ketonuria.

Echocardiography showed asymmetric LV wall thickening at end-diastole, predominantly involving the IVSd (8.5 mm; RI <6), with concurrent thickening of the LVFWd (7.5 mm), LA enlargement (LA:Ao 1.8) and reduced LA fractional shortening (8.5%). The LVIDd was below the RI at 10.2 mm (RI for a 6 kg cat 13.7–21.4) and the LVIDs was also decreased at 4.1 mm (RI for a 6 kg cat 6.1–14.1) (Table 1). No LV outflow tract obstruction was detected.

Thoracic radiographs demonstrated diffuse pulmonary infiltrates and pleural effusion, with changes compatible with cardiogenic pulmonary oedema (Figure 2). Approximately 25 ml of pleural fluid was removed and identified as a modified transudate. Treatment included oxygen supplementation, furosemide (2 mg/kg IV q12h), pimobendan (0.25 mg/kg PO q12h), clopidogrel (18.75 mg/cat PO q24h) and a dobutamine CRI (2.5 µg/kg/min), resulting in improvement in respiratory signs, radiographic pulmonary infiltrates and blood pressure. Glycaemic control was achieved with regular insulin (2 U IM q12h), which was later transitioned to glargine (2 U SC q12h). The cat stabilised and was discharged after an 8-day hospitalisation. IVSd remained increased (7.8 mm), while LVIDd had increased to 13.6 mm but remained below the RI.

Figure 2

Thoracic radiographs of case 2. At presentation, (a) right lateral and (b) ventrodorsal views show findings compatible with cardiogenic pulmonary oedema and suggest the presence of pleural effusion. At day 17, after congestive heart failure therapy and glycaemic control, (c) right lateral and (d) ventrodorsal views show resolution of pulmonary opacity and pleural changes, consistent with resolution of oedema and effusion

By day 17, the cat was clinically stable with no recurrence of respiratory distress while continuing cardiac medications and insulin therapy. Thoracic radiographs showed resolution of the pulmonary infiltrates and pleural effusion, with improvement in LA enlargement (Figure 2). Echocardiography demonstrated decreases in IVSd (8.5 to 5.8 mm) and LVFWd (7.5 to 4.0 mm), as well as LA:Ao (1.8 to 1.5), with LA fractional shortening improving to 29%. Blood glucose had decreased to 146 mg/dl and fructosamine had decreased to 212 µmol/l.

At day 135, the cat re-presented with dyspnoea. Both insulin and cardiac medications had been discontinued by the owner without veterinary instruction approximately 2 months prior, resulting in poor glycaemic control at home. Thoracic radiographs again demonstrated diffuse pulmonary infiltrates. Echocardiography showed an increase in myocardial thickness compared with the previous examination (IVSd 6.3 mm), along with an increase in LA:Ao (2.4) and a decrease in LA fractional shortening (16%) (Table 1). Marked hyperglycaemia (431 mg/dl) was present, and fructosamine had increased to 558 µmol/l (Table 2). The cat was hospitalised for 3 days and managed with treatment strategies similar to those used during the initial episode, resulting in clinical stabilisation. Intensive glycaemic control was then reinstated.

At day 180, myocardial thickness had again decreased (IVSd 5.8 mm), LA:Ao had decreased to 1.36 and LA fractional shortening improved to 32%. Representative echocardiographic images of case 2 are shown in Figure 3. NT-proBNP had decreased from 1367 pmol/l at presentation to below 50 pmol/l, blood glucose was 137 mg/dl and fructosamine was 331 µmol/l (Table 2). At 11 months after the initial event, the cat remained clinically stable. Both insulin therapy and cardiac medications had been gradually tapered and discontinued over several weeks after clinical stabilisation, with no recurrence of hyperglycaemia or echocardiographic deterioration during follow-up.

Figure 3

Echocardiographic images from case 2. (a) Short-axis view at the papillary muscle level at end-diastole and (b) the right parasternal short-axis view at the level of the aortic root at end-systole at the initial presentation, demonstrating LA enlargement and LV wall thickening. (c,d) The same views obtained 17 days later show a reduction in left atrial (LA) size and left ventricular (LV) wall thickness, consistent with improvement in cardiac remodelling after glycaemic control. (e,f) The same views obtained 135 days after the initial presentation reveal recurrence of LA enlargement and LV wall thickening, coinciding with worsening hyperglycaemia, consistent with worsening cardiac remodelling

Discussion

The occurrence and reversibility of CHF provide an important framework for interpreting these cases. TMT and other reversible cardiomyopathic changes have been reported in cats in association with inflammatory, stress-related, infectious and endocrine conditions.^3
–8 However, CHF associated with reversible myocardial changes in the context of poorly controlled DM has not been previously described. In both cats, clinical signs of CHF resolved after clinical stabilisation and optimisation of glycaemic management, accompanied by decreases in NT-proBNP concentrations and improvement in echocardiographic parameters.

In humans, diabetic cardiomyopathy is characterised by metabolic and cellular disturbances associated with hyperglycaemia and insulin deficiency, which may affect myocardial structure and function.^17,18 Clinical studies have shown that acute heart failure can improve after correction of severe hyperglycaemia, and early diabetic cardiomyopathy is considered partially reversible with appropriate glycaemic control.^19,20

In cats, previous studies have shown that DM is associated with an increased risk of developing heart failure.²¹ Furthermore, diabetic cats may exhibit diastolic dysfunction even in the absence of structural heart disease, supporting the possibility of diabetes-related myocardial dysfunction.²² In addition, necropsy findings in a diabetic cat with heart failure showed myocardial fibrosis with minimal myofibre disarray, suggesting a secondary rather than primary cardiomyopathy.²³

A similar pattern of myocardial remodelling has been described in cats with acromegaly, in which LV hypertrophy and diastolic dysfunction are common findings. These changes may be partially reversible after treatment, suggesting that endocrine-related myocardial changes can represent a secondary and potentially reversible form of cardiomyopathy.^24,25

In these two cases, resolution of CHF, together with decreases in myocardial thickness and improvements in echocardiographic findings after glycaemic stabilisation, suggests that metabolic dysregulation may influence cardiac structure and function in cats. These observations further indicate that effective glycaemic control, together with clinical stabilisation, may reduce the risk of recurrent CHF in diabetic cats.

Several limitations should be acknowledged. Complete historical information from the referring hospitals was not available. Both cats had reduced LV internal dimensions, raising the possibility of pseudohypertrophy related to dehydration;²⁶ however, the concurrent presence of LA enlargement and radiographic pulmonary infiltrates indicates that hypovolaemia alone may not fully account for the observed cardiac findings. In addition, stress-related hyperglycaemia associated with acute illness or heart failure cannot be excluded, and primary cardiomyopathy also remains a differential consideration, as myocardial wall thickness was within an equivocal range according to consensus guidelines.^2,27 Acromegaly was considered but was unlikely, given the rapid resolution of DM after insulin therapy and lack of characteristic clinical features.²⁸ Although IGF-1 testing was declined, the clinical course made this diagnosis improbable.

Conclusions

This case series describes two diabetic cats who presented with CHF and showed subsequent clinical improvement accompanied by partial regression of cardiac remodelling after optimisation of glycaemic management. These findings suggest a potential association between poorly controlled DM and reversible CHF in cats. Recognition of this possibility may support timely metabolic and cardiac management in affected patients.

Footnotes

Accepted: 15 April 2026

Conflict of interest

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

The work described in this manuscript involved the use of non-experimental (owned or unowned) animals. Established internationally recognised high standards (‘best practice’) of veterinary clinical care for the individual patient were always followed and/or this work involved the use of cadavers. Ethical approval from a committee was therefore not specifically required for publication in JFMS Open Reports. Although not required, where ethical approval was still obtained, it is stated in the manuscript.

Informed consent

Informed consent (verbal or written) was obtained from the owner or legal custodian of all animal(s) described in this work (experimental or non-experimental animals, including cadavers, tissues and samples) for all procedure(s) undertaken (prospective or retrospective studies). No animals or people are identifiable within this publication, and therefore additional informed consent for publication was not required.

ORCID iD

Jaechun Cho

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